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ATP + a peptide
ADP + a phosphorylated peptide
ATP + a protein
ADP + a phosphoprotein
ATP + a protein
ADP + phosphorylated protein
ATP + Akt
ADP + phosphorylated Akt
ATP + Arg-Lys-Arg-Ser-Arg-Ala-Glu
ADP + Arg-Lys-Arg-O-phospho-Ser-Arg-Ala-Glu
-
i.e. Glasstide, a commercial peptide substrate
-
-
?
ATP + BAD protein
ADP + BAD phosphoprotein
-
phosphorylation on Ser155 by PKG I
-
-
?
ATP + big potassium channel BKCa
ADP + phosphorylated big potassium channel BKCa
ATP + BKCa channel protein
ADP + BKCa channel phosphoprotein
ATP + BPDEtide
ADP + phosphorylated BPDEtide
-
-
-
-
?
ATP + CFTR
ADP + phosphorylated CFTR
ATP + CREb protein
ADP + phosphorylated CREb protein
-
-
-
-
?
ATP + cysteine-riche protein 2
ADP + phosphorylated vasodilator-stimulated phosphoprotein
ATP + DAPK2 protein
ADP + DAPK2 phosphoprotein
ATP + EKRKRTYETF
ADP + phosphorylated EKRKRTYETF
-
p65-derived synthetic peptide substrate
-
-
?
ATP + epidermal growth factor receptor
ADP + phosphorylated epidermal growth factor receptor
-
the enzyme phosphorylates epidermal growth factor receptor at threonine 669 and thereby inhibits its activation
-
-
?
ATP + FAM-GRTGRRNSI-NH2
ADP + phosphorylated FAM-GRTGRRNSI-NH2
ATP + FoxO1a
ADP + phosphorylated FoxO1a
ATP + GKKRKRSRKES
ADP + GKKRKRS(P)RKES
-
i.e. MCPD-4, a commercial peptide substrate
-
-
?
ATP + Glasstide
ADP + phosphorylated Glasstide
-
-
-
-
?
ATP + GluA1 protein
ADP + GluA1 phosphoprotein
ATP + glycogen synthase kinase-3
ADP + phosphorylated glycogen synthase kinase 3
-
phosphorylation at Ser9 by PKGI and PKGII inhibiting the glycogen synthase kinase-3 inducing dephosphorylation of C/EBPbeta, i.e. the CCAAT enhancer-binding protein beta, important in regulation of gene expression during cell proliferation, differentiation, and apoptosis
-
-
?
ATP + glycogen synthase kinase-3beta
ADP + phosphorylated glycogen synthase kinase-3beta
-
-
-
?
ATP + glycogen synthase kinase3
ADP + phosphorylated glycogen synthase kinase 3
-
phosphorylation at Ser9 by PKGI and PKGII inhibiting the glycogen synthase kinase-3, substrate phosphorylation site mapping
-
-
?
ATP + GRRESLTSFG
ADP + phosphorylated GRRESLTSFG
-
-
-
-
?
ATP + GRTGRRNSI
ADP + phosphorylated GRTGRRNSI
-
i.e. PKI, a commercial peptide substrate
-
-
?
ATP + GRTGRRNSI-amide
ADP + phosphorylated GRTGRRNSI-amide
-
assay substrate
-
-
?
ATP + GSK-3beta protein
ADP + GSK-3beta phosphoprotein
-
the enzyme phosphorylates GSK-3beta at serine-9 and inactivates it leading to the accumulation of beta-catenin and promoting the process of decidualization
-
-
?
ATP + HER2 protein
ADP + phosphorylated HER2 protein
-
phosphorylation at threonine 686
-
-
?
ATP + histone
ADP + phosphorylated histone
-
DG1
-
-
?
ATP + histone H1
ADP + phosphorylated histone H1
-
-
-
-
?
ATP + histone H2B
ADP + phosphorylated histone H2B
-
-
-
-
?
ATP + human serotonin transporter
ADP + phosphorylated human serotonin transporter
ATP + human serotonin transporter mutant I425V
ADP + phosphorylated human serotonin transporter mutant I425V
-
-
-
-
?
ATP + human serotonin transporter mutant T267A
ADP + phosphorylated human serotonin transporter mutant T267A
-
-
-
-
?
ATP + human serotonin transporter mutant T267A/I425V
ADP + phosphorylated human serotonin transporter mutant T267A/I425V
-
-
-
-
?
ATP + human serotonin transporter mutant T267D
ADP + phosphorylated human serotonin transporter mutant T267D
-
-
-
-
?
ATP + human serotonin transporter mutant T267D/I425V
ADP + phosphorylated human serotonin transporter mutant T267D/I425V
-
-
-
-
?
ATP + human serotonin transporter mutant T267E
ADP + phosphorylated human serotonin transporter mutant T267E
-
-
-
-
?
ATP + inositol 1,4,5-trisphosphate receptor-I
ADP + phosphorylated inositol 1,4,5-trisphosphate receptor-I
ATP + IRAG
ADP + phosphorylated IRAG
ATP + Kemptide
ADP + Kemptide phosphate
ATP + Kemptide
ADP + phosphorylated Kemptide
ATP + Maxi-K channel
ADP + phosphorylated Maxi-K channel
-
-
-
-
?
ATP + maxiK channel
ADP + phosphorylated maxiK channel
ATP + MQLRRPSDRE
ADP + phosphorylated MQLRRPSDRE
-
p65-derived synthetic peptide substrate
-
-
?
ATP + myosin phosphatase
ADP + phosphorylated RhoA
ATP + Na+/K+ ATPase
ADP + phosphorylated Na+/K+ ATPase
ATP + NF-kappaB
ADP + phosphorylated NF-kappaB
ATP + p21-activated kinase
ADP + phosphorylated p21-activated kinase
ATP + p65
ADP + phosphorylated p65
-
activity with recombinant wild-type p65 and mutants T305A and S276A
-
-
?
ATP + peptide W15
ADP + phosphorylated peptide W15
-
peptide substrate sequence TQAKRKKSLAMA
-
-
?
ATP + phosphodiesterase 5
ADP + phosphorylated phosphodiesterase 5
ATP + phospholamban
ADP + phosphorylated phospholamban
ATP + phospholipase Cbeta3
ADP + phosphorylated phospholipase Cbeta3
ATP + PKStide
ADP + phosphorylated PKStide
-
PKStide is GRTGRRNSI
-
-
?
ATP + protein
ADP + phosphoprotein
ATP + Rab11 protein
ADP + phosphorylated Rab11 protein
-
-
-
?
ATP + Rac1
ADP + phosphorylated Rac-1
ATP + Rho
ADP + phosphorylated rho
ATP + RhoA
ADP + phosphorylated RhoA
ATP + RKISASEFDRPL
ADP + phosphorylated RKISASEFDRPL
-
BPDEtide, substrate in activity assay
-
-
?
ATP + RKISASEFDRPLR
ADP + phosphorylated RKISASEFDRPLR
-
-
-
-
?
ATP + RKRSRAE
ADP + RKRS(P)RAE
ATP + septin 3
ADP + phosphorylated septin 3
ATP + septin 3 peptide 86-98
ADP + phosphorylated septin 3 peptide 86-98
-
-
-
-
?
ATP + serine/threonine protein
ADP + serine/threonine phosphorylated protein
-
-
-
-
?
ATP + steroidogenic acute regulatory protein
ADP + phosphorylated steroidogenic acute regulatory protein
-
i.e. StAR, recombinant GST-tagged substrate expressed in HEK-293 cells, phosphorylation in vitro at Ser55, Ser56, and Ser99
-
-
?
ATP + target membrane SNARe complex
ADP + phosphorylated target membrane SNARe complex
-
the enzyme is involved in regulation of degranulation of leukocytes by phosphorylation of target membrane SNARe complex together with the phosphoinositide 3-kinase
-
-
?
ATP + TPIalpha
ADP + phosphorylated TPIalpha
ATP + TQAKRKKSLAMA
ADP + phosphorylated TQAKRKKSLAMA
-
substrate in activity assay
-
-
?
ATP + transient receptor potential channel 6
ADP + phosphorylated transient receptor potential channel 6
ATP + TRAP protein
ADP + phosphorylated TRAP protein
-
-
-
-
?
ATP + TRIM39
ADP + phosphorylated TRIM39
ATP + TRIM39R
ADP + phosphorylated TRIM39R
ATP + troponin T
ADP + phosphorylated troponin T
ATP + TRPC3
ADP + phosphorylated TRPC3
ATP + vasodilator stimulated phosphoprotein
ADP + phosphorylated vasodilator stimulated phosphoprotein
ATP + vasodilator-stimulated phosphoprotein
ADP + phosphorylated vasodilator-stimulated phosphoprotein
ATP + VASP
ADP + VAS(P)P
-
-
-
-
?
ATP + VASP protein
ADP + phosphorylated VASP protein
additional information
?
-
ATP + a peptide
ADP + a phosphorylated peptide
-
-
-
-
?
ATP + a peptide
ADP + a phosphorylated peptide
-
-
-
-
?
ATP + a protein
ADP + a phosphoprotein
-
-
-
-
?
ATP + a protein
ADP + a phosphoprotein
-
-
-
-
?
ATP + a protein
ADP + a phosphoprotein
-
-
-
-
?
ATP + a protein
ADP + a phosphoprotein
-
-
-
-
?
ATP + a protein
ADP + phosphorylated protein
-
-
-
-
?
ATP + a protein
ADP + phosphorylated protein
-
-
-
?
ATP + a protein
ADP + phosphorylated protein
-
-
-
-
?
ATP + a protein
ADP + phosphorylated protein
-
-
-
-
?
ATP + Akt
ADP + phosphorylated Akt
-
-
-
-
?
ATP + Akt
ADP + phosphorylated Akt
-
phosphorylation at Ser473
-
-
?
ATP + big potassium channel BKCa
ADP + phosphorylated big potassium channel BKCa
-
phosphorylation by cGKI leads to activation of the channel, a mechanism leading to Ca2+-dependent smooth muscle relaxation
-
-
?
ATP + big potassium channel BKCa
ADP + phosphorylated big potassium channel BKCa
-
phosphorylation by cGKI
-
-
?
ATP + big potassium channel BKCa
ADP + phosphorylated big potassium channel BKCa
-
phosphorylation by cGKI leads to activation of the channel, a mechanism leading to Ca2+-dependent smooth muscle relaxation
-
-
?
ATP + big potassium channel BKCa
ADP + phosphorylated big potassium channel BKCa
-
phosphorylation by cGKI
-
-
?
ATP + BKCa channel protein
ADP + BKCa channel phosphoprotein
-
phosphorylation at mutiple serine residues, recombinant expressed Mus musculus BKCa channels
-
-
?
ATP + BKCa channel protein
ADP + BKCa channel phosphoprotein
-
phosphorylation at Ser691, Ser873, and Ser1112 on recombinant Mus musculus BKCa channels expressed in Rattus norvegicus aortic A7r5 smooth muscle cells or in humn in HEK 293 cells
-
-
?
ATP + CFTR
ADP + phosphorylated CFTR
-
phosphorylation leads to stimulation of chloride channels
-
-
?
ATP + CFTR
ADP + phosphorylated CFTR
-
phosphorylation by cGKI and cGKII
-
-
?
ATP + cysteine-riche protein 2
ADP + phosphorylated vasodilator-stimulated phosphoprotein
-
i.e. CRP2, phosphorylation by cGKI and cGKII
-
-
?
ATP + cysteine-riche protein 2
ADP + phosphorylated vasodilator-stimulated phosphoprotein
-
i.e. CRP2, phosphorylation by cGKI and cGKII
-
-
?
ATP + DAPK2 protein
ADP + DAPK2 phosphoprotein
-
i.e death-associated protein kinase 2, phosphorylation at Ser299, Ser367 and Ser368 type I cGMP-dependent protein kinase
-
-
?
ATP + DAPK2 protein
ADP + DAPK2 phosphoprotein
-
i.e death-associated protein kinase 2, phosphorylation at Ser299, Ser367 and Ser368 type I cGMP-dependent protein kinase, recombinant wild-type and mutant FLAG-tagged DAPK2 expressed in COS-7 cells, substrate detection from microarray substrate screening, overview
-
-
?
ATP + FAM-GRTGRRNSI-NH2
ADP + phosphorylated FAM-GRTGRRNSI-NH2
-
-
-
-
?
ATP + FAM-GRTGRRNSI-NH2
ADP + phosphorylated FAM-GRTGRRNSI-NH2
-
-
-
-
?
ATP + FAM-GRTGRRNSI-NH2
ADP + phosphorylated FAM-GRTGRRNSI-NH2
-
-
-
?
ATP + FAM-GRTGRRNSI-NH2
ADP + phosphorylated FAM-GRTGRRNSI-NH2
-
-
-
?
ATP + FAM-GRTGRRNSI-NH2
ADP + phosphorylated FAM-GRTGRRNSI-NH2
-
-
-
?
ATP + FoxO1a
ADP + phosphorylated FoxO1a
-
interaction of enzyme with FocO1a is involved in regulation of myoblast cell fusion during myogenesis
-
-
?
ATP + FoxO1a
ADP + phosphorylated FoxO1a
-
enzyme expression is activated by FoxO1a which is then phosphorylated by cGKI for feedback inhibition of FoxO1a DNA binding, phosphorylation of Ser152-155 and Ser184, and weakly of Ser266 and Ser268
-
-
?
ATP + GluA1 protein
ADP + GluA1 phosphoprotein
-
-
-
-
?
ATP + GluA1 protein
ADP + GluA1 phosphoprotein
-
phosphorylation at Ser845 by type II cGMP-dependent protein kinase
-
-
?
ATP + GluA1 protein
ADP + GluA1 phosphoprotein
-
phosphorylation at Ser845 by type II cGMP-dependent protein kinase
-
-
?
ATP + human serotonin transporter
ADP + phosphorylated human serotonin transporter
-
i.e. hSERT, the naturally occuring hSERT mutant I425V is associated with obsessive-compulsive disorder and other neuropsychiatric disorders
-
-
?
ATP + human serotonin transporter
ADP + phosphorylated human serotonin transporter
-
i.e. hSERT, no activity with hSERT mutants T276A or T276D, active with hSERT mutant I425V
-
-
?
ATP + inositol 1,4,5-trisphosphate receptor-I
ADP + phosphorylated inositol 1,4,5-trisphosphate receptor-I
-
the phosphorylation of the receptor inhibits inositol 1,4,5-trisphosphate-induced Ca2+ release
-
-
?
ATP + inositol 1,4,5-trisphosphate receptor-I
ADP + phosphorylated inositol 1,4,5-trisphosphate receptor-I
-
selective phosphorylation at Ser1755
-
-
?
ATP + IRAG
ADP + phosphorylated IRAG
-
phosphorylation by cGKIbeta mediates the inhibition of inositol-1,4,5-trisphosphate-dependent Ca2+-release, a mechanism leading to smooth muscle relaxation, involved in platelet aggregation
-
-
?
ATP + IRAG
ADP + phosphorylated IRAG
-
i.e. inositol-1,4,5-trisphosphate-receptor-associated cGMP kinase substrate, phosphorylation by cGKIbeta
-
-
?
ATP + IRAG
ADP + phosphorylated IRAG
-
i.e. inositol 1,4,5-trisphosphate receptor-associated cGMP kinase substrate, phosphorylation by isoyzme cGKIbeta, which is complexed with the substrate and the inositol 1,4,5-trisphosphate receptor in a ternary complex
-
-
?
ATP + IRAG
ADP + phosphorylated IRAG
-
i.e. inositol 1,4,5-trisphosphate receptor-associated cGMP kinase substrate, phosphorylation by isoyzme cGKIbeta
-
-
?
ATP + IRAG
ADP + phosphorylated IRAG
-
phosphorylation by cGKIbeta mediates the inhibition of inositol-1,4,5-trisphosphate-dependent Ca2+-release, one mechanism leading to smooth muscle relaxation, involved in platelet aggregation
-
-
?
ATP + IRAG
ADP + phosphorylated IRAG
-
i.e. inositol-1,4,5-trisphosphate-receptor-associated cGMP kinase substrate, phosphorylation by cGKIbeta
-
-
?
ATP + Kemptide
ADP + Kemptide phosphate
-
-
-
-
?
ATP + Kemptide
ADP + Kemptide phosphate
-
-
-
?
ATP + Kemptide
ADP + Kemptide phosphate
-
-
-
-
?
ATP + Kemptide
ADP + phosphorylated Kemptide
-
i.e. LRRASLG
i.e. LRRA-phosphoserine-LG
-
?
ATP + Kemptide
ADP + phosphorylated Kemptide
-
-
-
-
?
ATP + Kemptide
ADP + phosphorylated Kemptide
-
i.e. LRRASLG
i.e. LRRA-phosphoserine-LG
-
?
ATP + Kemptide
ADP + phosphorylated Kemptide
-
i.e. LRRASLG, a commercial peptide substrate
-
-
?
ATP + maxiK channel
ADP + phosphorylated maxiK channel
-
phosphorylation by isoyzme cGKI enhances the channel activity
-
-
?
ATP + maxiK channel
ADP + phosphorylated maxiK channel
-
phosphorylation of the PKC-phosphorylated substrate at Ser1072 by isoyzme cGKI
-
-
?
ATP + myosin phosphatase
ADP + phosphorylated RhoA
-
-
-
-
?
ATP + myosin phosphatase
ADP + phosphorylated RhoA
-
phosphorylation by isoyzme cGKIalpha leads to decreased level of phosphorylated MLC
-
-
?
ATP + myosin phosphatase
ADP + phosphorylated RhoA
-
i.e. MP, phosphorylation of the 130 kDa myosin-binding subunit by isoyzme cGKIalpha
-
-
?
ATP + Na+/K+ ATPase
ADP + phosphorylated Na+/K+ ATPase
-
-
-
-
?
ATP + Na+/K+ ATPase
ADP + phosphorylated Na+/K+ ATPase
-
the enzyme has a positive regulatory function on the ion pump activity induced by No and glutamate via increased cGMP, overview
-
-
?
ATP + NF-kappaB
ADP + phosphorylated NF-kappaB
-
recombinant human NF-kappaB p49 and p50 expressed in 293T cells
-
-
?
ATP + NF-kappaB
ADP + phosphorylated NF-kappaB
-
recombinant human NF-kappaB p49 and p50 expressed in 293T cells
-
-
?
ATP + p21-activated kinase
ADP + phosphorylated p21-activated kinase
-
PKG phosphorylation of p21-activated kinase, i.e. Pak, regulates HeLa cell and human umbilical vein endothelial cell morphology and cellular remodeling, time course of Pak1 activation in vivo, overview, PKG stimulates association of vasodilator-stimulated phosphoprotein VASP with Pak
-
-
?
ATP + p21-activated kinase
ADP + phosphorylated p21-activated kinase
-
activation of the wild-type p21-activated kinase, i.e. Pak1, PKG phosphorylates wild-type and mutant K299R Pak, PKG phosphorylates especially N-terminal amino acids 174, e.g. Ser21, and does not phosphorylate a fragment encompassing amino acids 67149 and only weakly phosphorylated fragments from the central region of Pak1 encompassing amino acids 147231 and the C-terminal catalytic region, amino acids 231544, no activity with Pak1 mutant S21A, overview
-
-
?
ATP + phosphodiesterase 5
ADP + phosphorylated phosphodiesterase 5
-
phosphorylation at Ser92 by isoyzme cGKI leads to enhanced hydrolysis of cGMP, regulatory function
-
-
?
ATP + phosphodiesterase 5
ADP + phosphorylated phosphodiesterase 5
-
phosphorylation at Ser92 by isoyzme cGKI
-
-
?
ATP + phospholamban
ADP + phosphorylated phospholamban
-
-
-
-
?
ATP + phospholamban
ADP + phosphorylated phospholamban
-
phosphorylation leads to stimulation of the sarcoendoplasmic reticulum pump Ca2+-ATPase, i.e. SERCA
-
-
?
ATP + phospholamban
ADP + phosphorylated phospholamban
-
-
-
-
?
ATP + phospholamban
ADP + phosphorylated phospholamban
-
phosphorylation leads to stimulation of the sarcoendoplasmic reticulum pump Ca2+-ATPase, i.e. SERCA
-
-
?
ATP + phospholipase Cbeta3
ADP + phosphorylated phospholipase Cbeta3
-
potentially involved in inhibition of phospholipase C activity
-
-
?
ATP + phospholipase Cbeta3
ADP + phosphorylated phospholipase Cbeta3
-
phosphorylation by cGKIbeta
-
-
?
ATP + protein
ADP + phosphoprotein
autophosphorylation
-
-
?
ATP + protein
ADP + phosphoprotein
autophosphorylation
-
-
?
ATP + Rac1
ADP + phosphorylated Rac-1
-
the enzyme activates the recombinant Myc-tagged small GTPase Rac1 in HEK-293 cells leading to activation of PAK1, the enzyme induces phosphorylation of p38 which activates MAPK, regulation, overview
-
-
?
ATP + Rac1
ADP + phosphorylated Rac-1
-
no activity with Rac-1 mutant T17N
-
-
?
ATP + Rho
ADP + phosphorylated rho
-
phosphorylation leads to inhibition of Rho
-
-
?
ATP + Rho
ADP + phosphorylated rho
-
a small GTP-binding protein, cGKI
-
-
?
ATP + Rho
ADP + phosphorylated rho
-
phosphorylation leads to inhibition of Rho
-
-
?
ATP + Rho
ADP + phosphorylated rho
-
a small GTP-binding protein, cGKI
-
-
?
ATP + RhoA
ADP + phosphorylated RhoA
-
phosphorylation at Ser188 by isoyzme cGKI leading to translocation of RhoA from the membrane to the cytosol and inactivates RhoA
-
-
?
ATP + RhoA
ADP + phosphorylated RhoA
-
phosphorylation at Ser188 by isoyzme cGKI
-
-
?
ATP + RKRSRAE
ADP + RKRS(P)RAE
-
cGK-specific peptide substrate
-
-
?
ATP + RKRSRAE
ADP + RKRS(P)RAE
-
commercial synthetic peptide substrate
-
-
?
ATP + septin 3
ADP + phosphorylated septin 3
-
substrate from rat nerves: recombinant His-tagged septin 3 expressed in Escherichia coli or purified from brain and prepared in synaptosomes, phosphorylation at Ser91 and Ser92, no activity with septin 3 mutants S91A and S92A
-
-
?
ATP + septin 3
ADP + phosphorylated septin 3
-
potentially involved in vesicle trafficking
-
-
?
ATP + septin 3
ADP + phosphorylated septin 3
-
phosphorylation by cGKIbeta
-
-
?
ATP + TPIalpha
ADP + phosphorylated TPIalpha
-
involved in desensitization of TPIalpha signalling
-
-
?
ATP + TPIalpha
ADP + phosphorylated TPIalpha
-
phosphorylation by cGKIbeta
-
-
?
ATP + transient receptor potential channel 6
ADP + phosphorylated transient receptor potential channel 6
-
PKG phosphorylation is reduced in transient receptor potential channel 6 mutant T69A
-
-
?
ATP + transient receptor potential channel 6
ADP + phosphorylated transient receptor potential channel 6
-
PKG phosphorylation is reduced in transient receptor potential channel 6 mutant T69A
-
-
?
ATP + TRIM39
ADP + phosphorylated TRIM39
-
-
-
-
?
ATP + TRIM39
ADP + phosphorylated TRIM39
-
phosphorylation of the tripartite motif protein 39 in the conserved phosphorylation domain by PKGI, recombinantly expresses TRIM39 substrate
-
-
?
ATP + TRIM39R
ADP + phosphorylated TRIM39R
-
PKGI interacts with TRIM39R, a Rpp21 domain-containing TRIM protein, in the kinase phosphorylation domain
-
-
?
ATP + TRIM39R
ADP + phosphorylated TRIM39R
-
phosphorylation of the endogenous putative PKGI-interactor and TRIM39 variant in the conserved phosphorylation domain by PKGI, recombinantly expresses TRIM39R substrate
-
-
?
ATP + troponin T
ADP + phosphorylated troponin T
-
phosphorylation by isoyzme cGKI in cardiomyocytes
-
-
?
ATP + troponin T
ADP + phosphorylated troponin T
-
phosphorylation by isoyzme cGKI
-
-
?
ATP + TRPC3
ADP + phosphorylated TRPC3
-
involved in inhibition of store operated Ca2+ influx
-
-
?
ATP + TRPC3
ADP + phosphorylated TRPC3
-
phosphorylation by cGKIbeta
-
-
?
ATP + vasodilator stimulated phosphoprotein
ADP + phosphorylated vasodilator stimulated phosphoprotein
-
-
-
-
?
ATP + vasodilator stimulated phosphoprotein
ADP + phosphorylated vasodilator stimulated phosphoprotein
-
phosphorylation of vasodilator stimulated phosphoprotein, i.e. VASP, induces detachment of VASP and other cytoskeletal proteins from focal adhesion, phosphorylated VASP may prevent dendritic cells from migrating towards CCl19
-
-
?
ATP + vasodilator stimulated phosphoprotein
ADP + phosphorylated vasodilator stimulated phosphoprotein
-
phosphorylation at Ser239
-
-
?
ATP + vasodilator-stimulated phosphoprotein
ADP + phosphorylated vasodilator-stimulated phosphoprotein
-
-
-
-
?
ATP + vasodilator-stimulated phosphoprotein
ADP + phosphorylated vasodilator-stimulated phosphoprotein
-
i.e. VASP, phosphorylation at Ser239 by cGKI
-
-
?
ATP + vasodilator-stimulated phosphoprotein
ADP + phosphorylated vasodilator-stimulated phosphoprotein
-
-
-
-
?
ATP + vasodilator-stimulated phosphoprotein
ADP + phosphorylated vasodilator-stimulated phosphoprotein
-
i.e. VASP, phosphorylation at Ser239 by cGKI
-
-
?
ATP + VASP protein
ADP + phosphorylated VASP protein
-
-
-
-
?
ATP + VASP protein
ADP + phosphorylated VASP protein
-
-
-
?
ATP + VASP protein
ADP + phosphorylated VASP protein
-
-
-
-
?
ATP + VASP protein
ADP + phosphorylated VASP protein
-
-
-
-
?
additional information
?
-
the enzyme is involved in age-dependent behavioural change from nurse to a foraging way of life by increased gene amfor expression
-
-
?
additional information
?
-
amino acid sequence at the ATP-binding site of cGMP-dependent protein kinase
-
-
?
additional information
?
-
-
guanylate cyclase and cyclic GMP-dependent protein kinase regulate agrin signaling at the postsynaptic differentiation of developing neuromuscular junctions, molecular mechanism
-
-
?
additional information
?
-
-
PKGIalpha is a major branch point in the nitric oxide and natriuretic peptide-induced cGMP-signaling pathway. PKG plays a pivotal role in several important biological processes such as the regulation of smooth muscle relaxation, and synaptic plasticity
-
-
?
additional information
?
-
-
peptide substrates with a primary amino acid sequence motif RRX(S/T)X are in general recognized by PKG
-
-
?
additional information
?
-
-
PKG phosphorylates several substrates and interacts, by engaging its N-terminal, with numerous proteins
-
-
?
additional information
?
-
-
PKG has an instructive signaling role to control many aspects of animal physiology
-
-
?
additional information
?
-
-
structure-function relationship of PKG
-
-
?
additional information
?
-
-
DG2P1 and DG2P2 are involved in behaviour and epithelial transport
-
-
?
additional information
?
-
the enzyme is involved in locomotion behaviour of the larvae in presence of food, so-called rover and sitter gene ecoding an isozyme termed forager, overview
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-
?
additional information
?
-
-
reduced enzyme activity leads to increased thermotolerance of synaptic transmission at the larval neuromuscular junction, PKG and the for gene polymorphism associated with the allelic variation in for may provide populationswith natural variantion in heat stress tolerance, the for gene function in behaviour is conserved across most organisms, overview
-
-
?
additional information
?
-
-
the enzyme PKG physically interacts with transcription factor LolaT both in vitro and in vivo
-
-
-
additional information
?
-
-
the enzyme is involved in coccidian parasite motility and invasion and is important in host-parasite interaction
-
-
?
additional information
?
-
the enzyme is involved in gliding motility and cell invasion
-
-
?
additional information
?
-
enzyme plays a crucial role in the relaxation of vascular smooth muscle by lowering the intracellular level of calcium
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-
?
additional information
?
-
-
enzyme plays a crucial role in the relaxation of vascular smooth muscle by lowering the intracellular level of calcium
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-
?
additional information
?
-
the enzyme is thought to be involved in the regulation of intestinal ion transport and fluid secretion
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-
?
additional information
?
-
-
the enzyme is thought to be involved in the regulation of intestinal ion transport and fluid secretion
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-
?
additional information
?
-
enzyme is involved in inhibition of platelet aggregation, relaxation of smooth muscle cells, and control of cardiocyte contractility. Pathophysiological implication of the type I cGK in cardiovascular diseases, including hypertension and atherosclerosis
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-
?
additional information
?
-
-
enzyme is involved in inhibition of platelet aggregation, relaxation of smooth muscle cells, and control of cardiocyte contractility. Pathophysiological implication of the type I cGK in cardiovascular diseases, including hypertension and atherosclerosis
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-
?
additional information
?
-
plays a pivotal role in the regulation of intestinal fluid balance in man
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-
?
additional information
?
-
-
plays a pivotal role in the regulation of intestinal fluid balance in man
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-
?
additional information
?
-
-
cGK is a key enzyme in the nitric oxide-cGMP and natriuretic signalling cascades, it modulates smooth muscle relaxation, platelet aggregation, renin release, intestinal secretion, learning amd memory, cGKII is involved in androsterone homeostasis, pleiotropic effets of the enzyme on diverse tissues, overview
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-
?
additional information
?
-
-
cGMP-activated PKGIalpha inhibits thrombin receptor-mediated Ca2+ mobilization in vascular smooth muscle cells, cGMP-activated PKGIbeta causes inhibition in vitro but has nearly no effect in vivo, the thrombin receptor is activated by thrombin receptor activating peptide TRAP, or lysophosphatidic acid, or U4, overview
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-
?
additional information
?
-
-
NO induces enzyme activity responsible for modulation/inhibition of voltage-gated CaV1 and CaV2.2, i.e. L- and N-type, Ca2+ channels in neuroblastoma cells, in cardiovascular and smooth muscle cells Ca2+ channel activity is inhibited by direct nitrosylation of the channel proteins by NO, overview
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-
?
additional information
?
-
-
sequential activation of p38 and ERK pathways by the enzyme leading to activation of the platelet integrin alphaIIb beta3
-
-
?
additional information
?
-
-
the enzyme mediates an exocytosis pathway via glycoprotein Ib-IX, and an aggregation-dependent platelet secretion pathway important for amplifying platelet activation, in stabilizing thrombi, and in arteriosclerosis and vascular remodeling, signaling mechanism activating the enzyme, overview
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-
?
additional information
?
-
-
the enzyme negatively regulates gene expression of thrombospondin 1, which activates the transforming growth factor-beta, at both transcriptional and posttranscriptional level inhibiting the fibrogenic potential fo high D-glucose levels, overview
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-
?
additional information
?
-
-
the enzyme performs autophosphorylation at serines 110, 114, 117, 126, and 445 and at Thr109 in vitro and in vivo
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-
?
additional information
?
-
-
the NO/cGMP pathway including inhibits Ca2+-dependent and turbulence-induced Rap 1 activation in human platelets mediated by cGKI in platelets and megakaryocytes
-
-
?
additional information
?
-
-
through its c-Myc-, AP-1- and PEA3-binding motifs the enzyme regulates the expression of thioredoxin and thioredoxin peroxidase-1 during hormesis in response to oxidative stress-induced apoptosis, the enzyme is involved in cell protection against apoptosis and lipid oxidation
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-
?
additional information
?
-
-
NO and cGMP protein kinase regulate dendritic-cell migration toward the lymph-node-directing chemokine CCL19, cGMP/cGK pathway, overview
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-
?
additional information
?
-
-
PKG Ialpha attenuates necrosis and apoptosis following ischemia/reoxygenation in adult cardiomyocyte, overview
-
-
?
additional information
?
-
-
PKG inhibits p38 MAPK activation in platelets
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-
?
additional information
?
-
-
PKGI, in part, mediates the regulation of pulmonary cell proliferation and phenotype caused by NO and cGMP, in cells that lack PKGI such as highly passaged vascular smooth muscle cells, NO and cGMP do not regulate cell proliferation and phenotype
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-
?
additional information
?
-
-
the enzyme is involved in development of anoikis, an essential process in which a loss of adhesion to the substratum alters intracellular signaling pathways that lead to apoptosis
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-
?
additional information
?
-
-
transcriptional regulation by the cgMP/PKG pathway affects the amount of IL-6 expression, cGMP-induced PKG activates the IL-6 promoter involving cis-acting DNA elements and transcription factors, the activation is prevented by actinomycin D, regulation system, overview
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-
?
additional information
?
-
-
PKG phosphorylates several substrates and interacts, by engaging its N-terminal, with numerous proteins
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-
?
additional information
?
-
-
isozymes cGK I and cGK II are functionally distinct, isozyme cGK II is involved in regulation of electrolyte and water secretion by epithelial tissues in response to luminocrinic hormones guanylin and uroguanylin and in the secretory diarrhea provoked by heat-stable enterotoxins, isozyme cGK II also plays a role in the regulation of endochondral ossification by C-type natriuretic peptide, in renin secretion by the kidney, aldosterone secretion by the adrenal, and adjustment of the biological clock
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?
additional information
?
-
-
the enzyme activates diverse signal transduction pathways, isozyme cGKI is responsible for smooth muscle relaxation by lowering the cytosolic calcium level and/or by desensitization of the contractile elements, smooth muscle contraction and enzyme-mediated smooth muscle relaxation mechanisms, detailed overview, cGKI affects the Ca2+ efflux from the endoplasmic reticulum and the cytosolic Ca2+ concentration
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-
?
additional information
?
-
-
cGK is a key enzyme in the nitric oxide-cGMP and natriuretic signalling cascades, it modulates smooth muscle relaxation, platelet aggregation, renin release, intestinal secretion, learning amd memory, cGKII is involved in androsterone homeostasis, pleiotropic effets of the enzyme on diverse tissues, overview
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?
additional information
?
-
-
cGKI mediates NO signaling and plays a proatherogenic role in vascular smooth muscle cells, enzyme activation in primary smoothe muscle cells results in increased levels of proliferation and vascular cell adhesion molecule-1, peroxisome proliferato-activated receptor gamma, and phosphatidylinositol 3-kinase/Akt signaling, and in decreased plasminogen activator inhibitor 1 mRNA, overview
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-
?
additional information
?
-
-
PKGII modulates mPer1 and mPer2 gene induction, not by phosphorylation of CREB at Ser133, and influences phase shifts of the circadian clock, regulation model, overview
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-
?
additional information
?
-
-
sequential activation of p38 and ERK pathways by the enzyme leading to activation of the platelet integrin alphaIIb beta3
-
-
?
additional information
?
-
-
the enzyme mediates an exocytosis pathway via glycoprotein Ib-IX, and an aggregation-dependent platelet secretion pathway important for amplifying platelet activation, in stabilizing thrombi, and in arteriosclerosis and vascular remodeling, signaling mechanism activating the enzyme, overview
-
-
?
additional information
?
-
-
the enzyme mediates NO- but not acetylcholine-induced dilations in resistance vessels in vivo
-
-
?
additional information
?
-
-
the enzyme performs autophosphorylation at serines 110, 114, 117, 126, and 445 and at Thr109 in vitro and in vivo
-
-
?
additional information
?
-
-
no activity with the cAMP-responsive element binding protein, i.e. CREB
-
-
?
additional information
?
-
-
cGMP-activated PKGI inhibits TAB1-p38 mitogen-activated protein kinase apoptosis signaling in cardiac myocytes and protects them from ischemia and reperfusion injury, cGMP-activated PKG I does not inhibit MKK3- and MKK6-p38 MAPK signaling, overview
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-
?
additional information
?
-
the cGMP/cGMP-dependent protein kinase I signaling pathway plays an important role in spinal nociceptive processing and interacts with cysteine-rich protein 2
-
-
?
additional information
?
-
-
PKG phosphorylates several substrates and interacts, by engaging its N-terminal, with numerous proteins
-
-
?
additional information
?
-
-
cGMP-activated PKGI inhibits TAB1-p38 mitogen-activated protein kinase apoptosis signaling in cardiac myocytes and protects them from ischemia and reperfusion injury, cGMP-activated PKG I does not inhibit MKK3- and MKK6-p38 MAPK signaling, overview
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-
?
additional information
?
-
-
PKG-1 is involved in NO-induced cGMP-mediated increase in corpus cavernosum smooth muscle relaxation and penile erection, enzyme disfunction can cause erectile dysfunction, diabetes reduces corpus cavernosum smooth muscle relaxation
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?
additional information
?
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-
PKG phosphorylates several substrates and interacts, by engaging its N-terminal, with numerous proteins
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-
?
additional information
?
-
-
PKG phosphorylates several substrates and interacts, by engaging its N-terminal, with numerous proteins
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-
?
additional information
?
-
the enzyme is involved in cGMP-dependent male gametogenesis, i.e. exflagellation, together with Ca2+ release
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-
?
additional information
?
-
the enzyme is involved in cGMP-dependent male gametogenesis, i.e. exflagellation, together with Ca2+ release
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?
additional information
?
-
-
the enzyme is involved in cGMP-dependent male gametogenesis, i.e. exflagellation, together with Ca2+ release
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?
additional information
?
-
-
PKG is essential for xanthurenic acid- and zaprinast-induced gametogenesis in Plasmodium falciparum
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-
?
additional information
?
-
-
global protein phosphorylation pattern of schizonts, overview
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-
?
additional information
?
-
-
alternative splicing of PKGI in angiotensin-hypertension, mechanism for nitrate tolerance in vascular smooth muscle
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-
?
additional information
?
-
-
cyclic GMP-dependent protein kinase regulates CCAAT enhancer-binding protein beta functions through inhibition of glycogen synthase kinase-3
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-
?
additional information
?
-
-
PKGII regulates basal level of aldosterone production by zona glomerulosa cells without increasing expression of the steroidogenic acute regulatory protein gene
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-
?
additional information
?
-
-
the enzyme is required for adenosine-induced dilation of intracerebral arterioles and thus in regulation of cerebral blood flow, mechanism
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-
?
additional information
?
-
-
the enzyme performs autophosphorylation at serines 110, 114, 117, 126, and 445 and at Thr109 in vitro and in vivo
-
-
?
additional information
?
-
-
the phorbol myristate acetate-stimulated PKC isozyme activates BKCa channels in rat pulmonary arterial smooth muscle via cGMP-dependent protein kinase
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-
?
additional information
?
-
-
cGMP-activated PKGI inhibits TAB1-p38 mitogen-activated protein kinase apoptosis signaling in cardiac myocytes and protects them from ischemia and reperfusion injury, cGMP-activated PKG I does not inhibit MKK3- and MKK6-p38 MAPK signaling, overview
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-
?
additional information
?
-
-
PKG I plays a major role in vascular homeostasis by mediating smooth muscle relaxation in response to nitric oxide, regulation of PKG I expression by Rho and Kruppel-like transcription factor-4, RhoA is involved in decreased PKG I levels in vascular smooth muscle cells found in some models of hypertension and vascular injury, overview
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-
?
additional information
?
-
-
transcriptional regulation by the cgMP/PKG pathway affects the amount of IL-6 expression, cGMP-induced PKG activates the IL-6 promoter involving cis-acting DNA elements and transcription factors, the activation is prevented by actinomycin D, regulation system, overview
-
-
?
additional information
?
-
-
PKG phosphorylates several substrates and interacts, by engaging its N-terminal, with numerous proteins
-
-
?
additional information
?
-
-
serine to alanine substitutions at 3 of 6 putative cGKI phosphorylation sites, Ser691, Ser873, and Ser1112, in the BKCa alpha-subunit and mutant expression in A7r5 cells individually reduce direct channel phosphorylation by 25-60% and block BKCa activation by either an NO donor or a membrane-permeable cGMP by 80-100%
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?
additional information
?
-
-
PKG is involved in the regulation of basal tension and plays a primary role in relaxation induced by nitrovasodilators, whereas PKA may play a minor role
-
-
?
additional information
?
-
-
PKG phosphorylates several substrates and interacts, by engaging its N-terminal, with numerous proteins
-
-
?
additional information
?
-
-
the enzyme is involved in coccidian parasite motility and invasion and is important in host-parasite interaction
-
-
?
additional information
?
-
Q8MMP4
the enzyme is involved in gliding motility and cell invasion
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?
Please wait a moment until the data is sorted. This message will disappear when the data is sorted.
ATP + a protein
ADP + a phosphoprotein
ATP + a protein
ADP + phosphorylated protein
ATP + Akt
ADP + phosphorylated Akt
-
-
-
-
?
ATP + BAD protein
ADP + BAD phosphoprotein
-
phosphorylation on Ser155 by PKG I
-
-
?
ATP + big potassium channel BKCa
ADP + phosphorylated big potassium channel BKCa
ATP + CFTR
ADP + phosphorylated CFTR
-
phosphorylation leads to stimulation of chloride channels
-
-
?
ATP + CREb protein
ADP + phosphorylated CREb protein
-
-
-
-
?
ATP + cysteine-riche protein 2
ADP + phosphorylated vasodilator-stimulated phosphoprotein
ATP + DAPK2 protein
ADP + DAPK2 phosphoprotein
-
i.e death-associated protein kinase 2, phosphorylation at Ser299, Ser367 and Ser368 type I cGMP-dependent protein kinase
-
-
?
ATP + epidermal growth factor receptor
ADP + phosphorylated epidermal growth factor receptor
-
the enzyme phosphorylates epidermal growth factor receptor at threonine 669 and thereby inhibits its activation
-
-
?
ATP + FoxO1a
ADP + phosphorylated FoxO1a
-
interaction of enzyme with FocO1a is involved in regulation of myoblast cell fusion during myogenesis
-
-
?
ATP + GluA1 protein
ADP + GluA1 phosphoprotein
ATP + glycogen synthase kinase-3
ADP + phosphorylated glycogen synthase kinase 3
-
phosphorylation at Ser9 by PKGI and PKGII inhibiting the glycogen synthase kinase-3 inducing dephosphorylation of C/EBPbeta, i.e. the CCAAT enhancer-binding protein beta, important in regulation of gene expression during cell proliferation, differentiation, and apoptosis
-
-
?
ATP + GSK-3beta protein
ADP + GSK-3beta phosphoprotein
-
the enzyme phosphorylates GSK-3beta at serine-9 and inactivates it leading to the accumulation of beta-catenin and promoting the process of decidualization
-
-
?
ATP + HER2 protein
ADP + phosphorylated HER2 protein
-
phosphorylation at threonine 686
-
-
?
ATP + human serotonin transporter
ADP + phosphorylated human serotonin transporter
-
i.e. hSERT, the naturally occuring hSERT mutant I425V is associated with obsessive-compulsive disorder and other neuropsychiatric disorders
-
-
?
ATP + inositol 1,4,5-trisphosphate receptor-I
ADP + phosphorylated inositol 1,4,5-trisphosphate receptor-I
-
the phosphorylation of the receptor inhibits inositol 1,4,5-trisphosphate-induced Ca2+ release
-
-
?
ATP + IRAG
ADP + phosphorylated IRAG
ATP + Kemptide
ADP + Kemptide phosphate
ATP + maxiK channel
ADP + phosphorylated maxiK channel
-
phosphorylation by isoyzme cGKI enhances the channel activity
-
-
?
ATP + myosin phosphatase
ADP + phosphorylated RhoA
-
phosphorylation by isoyzme cGKIalpha leads to decreased level of phosphorylated MLC
-
-
?
ATP + Na+/K+ ATPase
ADP + phosphorylated Na+/K+ ATPase
-
the enzyme has a positive regulatory function on the ion pump activity induced by No and glutamate via increased cGMP, overview
-
-
?
ATP + p21-activated kinase
ADP + phosphorylated p21-activated kinase
-
PKG phosphorylation of p21-activated kinase, i.e. Pak, regulates HeLa cell and human umbilical vein endothelial cell morphology and cellular remodeling, time course of Pak1 activation in vivo, overview, PKG stimulates association of vasodilator-stimulated phosphoprotein VASP with Pak
-
-
?
ATP + phosphodiesterase 5
ADP + phosphorylated phosphodiesterase 5
-
phosphorylation at Ser92 by isoyzme cGKI leads to enhanced hydrolysis of cGMP, regulatory function
-
-
?
ATP + phospholamban
ADP + phosphorylated phospholamban
ATP + phospholipase Cbeta3
ADP + phosphorylated phospholipase Cbeta3
-
potentially involved in inhibition of phospholipase C activity
-
-
?
ATP + Rab11 protein
ADP + phosphorylated Rab11 protein
-
-
-
?
ATP + Rac1
ADP + phosphorylated Rac-1
-
the enzyme activates the recombinant Myc-tagged small GTPase Rac1 in HEK-293 cells leading to activation of PAK1, the enzyme induces phosphorylation of p38 which activates MAPK, regulation, overview
-
-
?
ATP + Rho
ADP + phosphorylated rho
ATP + RhoA
ADP + phosphorylated RhoA
-
phosphorylation at Ser188 by isoyzme cGKI leading to translocation of RhoA from the membrane to the cytosol and inactivates RhoA
-
-
?
ATP + septin 3
ADP + phosphorylated septin 3
-
potentially involved in vesicle trafficking
-
-
?
ATP + target membrane SNARe complex
ADP + phosphorylated target membrane SNARe complex
-
the enzyme is involved in regulation of degranulation of leukocytes by phosphorylation of target membrane SNARe complex together with the phosphoinositide 3-kinase
-
-
?
ATP + TPIalpha
ADP + phosphorylated TPIalpha
-
involved in desensitization of TPIalpha signalling
-
-
?
ATP + TRAP protein
ADP + phosphorylated TRAP protein
-
-
-
-
?
ATP + TRIM39
ADP + phosphorylated TRIM39
-
-
-
-
?
ATP + TRIM39R
ADP + phosphorylated TRIM39R
-
PKGI interacts with TRIM39R, a Rpp21 domain-containing TRIM protein, in the kinase phosphorylation domain
-
-
?
ATP + troponin T
ADP + phosphorylated troponin T
-
phosphorylation by isoyzme cGKI in cardiomyocytes
-
-
?
ATP + TRPC3
ADP + phosphorylated TRPC3
-
involved in inhibition of store operated Ca2+ influx
-
-
?
ATP + vasodilator stimulated phosphoprotein
ADP + phosphorylated vasodilator stimulated phosphoprotein
ATP + vasodilator-stimulated phosphoprotein
ADP + phosphorylated vasodilator-stimulated phosphoprotein
ATP + VASP protein
ADP + phosphorylated VASP protein
-
-
-
-
?
additional information
?
-
ATP + a protein
ADP + a phosphoprotein
-
-
-
-
?
ATP + a protein
ADP + a phosphoprotein
-
-
-
-
?
ATP + a protein
ADP + a phosphoprotein
-
-
-
-
?
ATP + a protein
ADP + a phosphoprotein
-
-
-
-
?
ATP + a protein
ADP + phosphorylated protein
-
-
-
-
?
ATP + a protein
ADP + phosphorylated protein
-
-
-
?
ATP + a protein
ADP + phosphorylated protein
-
-
-
-
?
ATP + a protein
ADP + phosphorylated protein
-
-
-
-
?
ATP + big potassium channel BKCa
ADP + phosphorylated big potassium channel BKCa
-
phosphorylation by cGKI leads to activation of the channel, a mechanism leading to Ca2+-dependent smooth muscle relaxation
-
-
?
ATP + big potassium channel BKCa
ADP + phosphorylated big potassium channel BKCa
-
phosphorylation by cGKI leads to activation of the channel, a mechanism leading to Ca2+-dependent smooth muscle relaxation
-
-
?
ATP + cysteine-riche protein 2
ADP + phosphorylated vasodilator-stimulated phosphoprotein
-
i.e. CRP2, phosphorylation by cGKI and cGKII
-
-
?
ATP + cysteine-riche protein 2
ADP + phosphorylated vasodilator-stimulated phosphoprotein
-
i.e. CRP2, phosphorylation by cGKI and cGKII
-
-
?
ATP + GluA1 protein
ADP + GluA1 phosphoprotein
-
-
-
-
?
ATP + GluA1 protein
ADP + GluA1 phosphoprotein
-
phosphorylation at Ser845 by type II cGMP-dependent protein kinase
-
-
?
ATP + GluA1 protein
ADP + GluA1 phosphoprotein
-
phosphorylation at Ser845 by type II cGMP-dependent protein kinase
-
-
?
ATP + IRAG
ADP + phosphorylated IRAG
-
phosphorylation by cGKIbeta mediates the inhibition of inositol-1,4,5-trisphosphate-dependent Ca2+-release, a mechanism leading to smooth muscle relaxation, involved in platelet aggregation
-
-
?
ATP + IRAG
ADP + phosphorylated IRAG
-
i.e. inositol 1,4,5-trisphosphate receptor-associated cGMP kinase substrate, phosphorylation by isoyzme cGKIbeta, which is complexed with the substrate and the inositol 1,4,5-trisphosphate receptor in a ternary complex
-
-
?
ATP + IRAG
ADP + phosphorylated IRAG
-
phosphorylation by cGKIbeta mediates the inhibition of inositol-1,4,5-trisphosphate-dependent Ca2+-release, one mechanism leading to smooth muscle relaxation, involved in platelet aggregation
-
-
?
ATP + Kemptide
ADP + Kemptide phosphate
-
-
-
?
ATP + Kemptide
ADP + Kemptide phosphate
-
-
-
-
?
ATP + phospholamban
ADP + phosphorylated phospholamban
-
phosphorylation leads to stimulation of the sarcoendoplasmic reticulum pump Ca2+-ATPase, i.e. SERCA
-
-
?
ATP + phospholamban
ADP + phosphorylated phospholamban
-
phosphorylation leads to stimulation of the sarcoendoplasmic reticulum pump Ca2+-ATPase, i.e. SERCA
-
-
?
ATP + Rho
ADP + phosphorylated rho
-
phosphorylation leads to inhibition of Rho
-
-
?
ATP + Rho
ADP + phosphorylated rho
-
phosphorylation leads to inhibition of Rho
-
-
?
ATP + vasodilator stimulated phosphoprotein
ADP + phosphorylated vasodilator stimulated phosphoprotein
-
-
-
-
?
ATP + vasodilator stimulated phosphoprotein
ADP + phosphorylated vasodilator stimulated phosphoprotein
-
phosphorylation of vasodilator stimulated phosphoprotein, i.e. VASP, induces detachment of VASP and other cytoskeletal proteins from focal adhesion, phosphorylated VASP may prevent dendritic cells from migrating towards CCl19
-
-
?
ATP + vasodilator-stimulated phosphoprotein
ADP + phosphorylated vasodilator-stimulated phosphoprotein
-
-
-
-
?
ATP + vasodilator-stimulated phosphoprotein
ADP + phosphorylated vasodilator-stimulated phosphoprotein
-
-
-
-
?
additional information
?
-
the enzyme is involved in age-dependent behavioural change from nurse to a foraging way of life by increased gene amfor expression
-
-
?
additional information
?
-
amino acid sequence at the ATP-binding site of cGMP-dependent protein kinase
-
-
?
additional information
?
-
-
guanylate cyclase and cyclic GMP-dependent protein kinase regulate agrin signaling at the postsynaptic differentiation of developing neuromuscular junctions, molecular mechanism
-
-
?
additional information
?
-
-
PKGIalpha is a major branch point in the nitric oxide and natriuretic peptide-induced cGMP-signaling pathway. PKG plays a pivotal role in several important biological processes such as the regulation of smooth muscle relaxation, and synaptic plasticity
-
-
?
additional information
?
-
-
PKG phosphorylates several substrates and interacts, by engaging its N-terminal, with numerous proteins
-
-
?
additional information
?
-
-
PKG has an instructive signaling role to control many aspects of animal physiology
-
-
?
additional information
?
-
-
DG2P1 and DG2P2 are involved in behaviour and epithelial transport
-
-
?
additional information
?
-
the enzyme is involved in locomotion behaviour of the larvae in presence of food, so-called rover and sitter gene ecoding an isozyme termed forager, overview
-
-
?
additional information
?
-
-
reduced enzyme activity leads to increased thermotolerance of synaptic transmission at the larval neuromuscular junction, PKG and the for gene polymorphism associated with the allelic variation in for may provide populationswith natural variantion in heat stress tolerance, the for gene function in behaviour is conserved across most organisms, overview
-
-
?
additional information
?
-
-
the enzyme is involved in coccidian parasite motility and invasion and is important in host-parasite interaction
-
-
?
additional information
?
-
the enzyme is involved in gliding motility and cell invasion
-
-
?
additional information
?
-
enzyme plays a crucial role in the relaxation of vascular smooth muscle by lowering the intracellular level of calcium
-
-
?
additional information
?
-
-
enzyme plays a crucial role in the relaxation of vascular smooth muscle by lowering the intracellular level of calcium
-
-
?
additional information
?
-
the enzyme is thought to be involved in the regulation of intestinal ion transport and fluid secretion
-
-
?
additional information
?
-
-
the enzyme is thought to be involved in the regulation of intestinal ion transport and fluid secretion
-
-
?
additional information
?
-
enzyme is involved in inhibition of platelet aggregation, relaxation of smooth muscle cells, and control of cardiocyte contractility. Pathophysiological implication of the type I cGK in cardiovascular diseases, including hypertension and atherosclerosis
-
-
?
additional information
?
-
-
enzyme is involved in inhibition of platelet aggregation, relaxation of smooth muscle cells, and control of cardiocyte contractility. Pathophysiological implication of the type I cGK in cardiovascular diseases, including hypertension and atherosclerosis
-
-
?
additional information
?
-
plays a pivotal role in the regulation of intestinal fluid balance in man
-
-
?
additional information
?
-
-
plays a pivotal role in the regulation of intestinal fluid balance in man
-
-
?
additional information
?
-
-
cGK is a key enzyme in the nitric oxide-cGMP and natriuretic signalling cascades, it modulates smooth muscle relaxation, platelet aggregation, renin release, intestinal secretion, learning amd memory, cGKII is involved in androsterone homeostasis, pleiotropic effets of the enzyme on diverse tissues, overview
-
-
?
additional information
?
-
-
cGMP-activated PKGIalpha inhibits thrombin receptor-mediated Ca2+ mobilization in vascular smooth muscle cells, cGMP-activated PKGIbeta causes inhibition in vitro but has nearly no effect in vivo, the thrombin receptor is activated by thrombin receptor activating peptide TRAP, or lysophosphatidic acid, or U4, overview
-
-
?
additional information
?
-
-
NO induces enzyme activity responsible for modulation/inhibition of voltage-gated CaV1 and CaV2.2, i.e. L- and N-type, Ca2+ channels in neuroblastoma cells, in cardiovascular and smooth muscle cells Ca2+ channel activity is inhibited by direct nitrosylation of the channel proteins by NO, overview
-
-
?
additional information
?
-
-
sequential activation of p38 and ERK pathways by the enzyme leading to activation of the platelet integrin alphaIIb beta3
-
-
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additional information
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the enzyme mediates an exocytosis pathway via glycoprotein Ib-IX, and an aggregation-dependent platelet secretion pathway important for amplifying platelet activation, in stabilizing thrombi, and in arteriosclerosis and vascular remodeling, signaling mechanism activating the enzyme, overview
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?
additional information
?
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the enzyme negatively regulates gene expression of thrombospondin 1, which activates the transforming growth factor-beta, at both transcriptional and posttranscriptional level inhibiting the fibrogenic potential fo high D-glucose levels, overview
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?
additional information
?
-
-
the enzyme performs autophosphorylation at serines 110, 114, 117, 126, and 445 and at Thr109 in vitro and in vivo
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?
additional information
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the NO/cGMP pathway including inhibits Ca2+-dependent and turbulence-induced Rap 1 activation in human platelets mediated by cGKI in platelets and megakaryocytes
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?
additional information
?
-
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through its c-Myc-, AP-1- and PEA3-binding motifs the enzyme regulates the expression of thioredoxin and thioredoxin peroxidase-1 during hormesis in response to oxidative stress-induced apoptosis, the enzyme is involved in cell protection against apoptosis and lipid oxidation
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?
additional information
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NO and cGMP protein kinase regulate dendritic-cell migration toward the lymph-node-directing chemokine CCL19, cGMP/cGK pathway, overview
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?
additional information
?
-
-
PKG Ialpha attenuates necrosis and apoptosis following ischemia/reoxygenation in adult cardiomyocyte, overview
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?
additional information
?
-
-
PKG inhibits p38 MAPK activation in platelets
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?
additional information
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PKGI, in part, mediates the regulation of pulmonary cell proliferation and phenotype caused by NO and cGMP, in cells that lack PKGI such as highly passaged vascular smooth muscle cells, NO and cGMP do not regulate cell proliferation and phenotype
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?
additional information
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the enzyme is involved in development of anoikis, an essential process in which a loss of adhesion to the substratum alters intracellular signaling pathways that lead to apoptosis
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additional information
?
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transcriptional regulation by the cgMP/PKG pathway affects the amount of IL-6 expression, cGMP-induced PKG activates the IL-6 promoter involving cis-acting DNA elements and transcription factors, the activation is prevented by actinomycin D, regulation system, overview
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?
additional information
?
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-
PKG phosphorylates several substrates and interacts, by engaging its N-terminal, with numerous proteins
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?
additional information
?
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isozymes cGK I and cGK II are functionally distinct, isozyme cGK II is involved in regulation of electrolyte and water secretion by epithelial tissues in response to luminocrinic hormones guanylin and uroguanylin and in the secretory diarrhea provoked by heat-stable enterotoxins, isozyme cGK II also plays a role in the regulation of endochondral ossification by C-type natriuretic peptide, in renin secretion by the kidney, aldosterone secretion by the adrenal, and adjustment of the biological clock
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additional information
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the enzyme activates diverse signal transduction pathways, isozyme cGKI is responsible for smooth muscle relaxation by lowering the cytosolic calcium level and/or by desensitization of the contractile elements, smooth muscle contraction and enzyme-mediated smooth muscle relaxation mechanisms, detailed overview, cGKI affects the Ca2+ efflux from the endoplasmic reticulum and the cytosolic Ca2+ concentration
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additional information
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cGK is a key enzyme in the nitric oxide-cGMP and natriuretic signalling cascades, it modulates smooth muscle relaxation, platelet aggregation, renin release, intestinal secretion, learning amd memory, cGKII is involved in androsterone homeostasis, pleiotropic effets of the enzyme on diverse tissues, overview
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additional information
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cGKI mediates NO signaling and plays a proatherogenic role in vascular smooth muscle cells, enzyme activation in primary smoothe muscle cells results in increased levels of proliferation and vascular cell adhesion molecule-1, peroxisome proliferato-activated receptor gamma, and phosphatidylinositol 3-kinase/Akt signaling, and in decreased plasminogen activator inhibitor 1 mRNA, overview
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?
additional information
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PKGII modulates mPer1 and mPer2 gene induction, not by phosphorylation of CREB at Ser133, and influences phase shifts of the circadian clock, regulation model, overview
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additional information
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-
-
sequential activation of p38 and ERK pathways by the enzyme leading to activation of the platelet integrin alphaIIb beta3
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?
additional information
?
-
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the enzyme mediates an exocytosis pathway via glycoprotein Ib-IX, and an aggregation-dependent platelet secretion pathway important for amplifying platelet activation, in stabilizing thrombi, and in arteriosclerosis and vascular remodeling, signaling mechanism activating the enzyme, overview
-
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?
additional information
?
-
-
the enzyme mediates NO- but not acetylcholine-induced dilations in resistance vessels in vivo
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?
additional information
?
-
-
the enzyme performs autophosphorylation at serines 110, 114, 117, 126, and 445 and at Thr109 in vitro and in vivo
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?
additional information
?
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cGMP-activated PKGI inhibits TAB1-p38 mitogen-activated protein kinase apoptosis signaling in cardiac myocytes and protects them from ischemia and reperfusion injury, cGMP-activated PKG I does not inhibit MKK3- and MKK6-p38 MAPK signaling, overview
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-
?
additional information
?
-
the cGMP/cGMP-dependent protein kinase I signaling pathway plays an important role in spinal nociceptive processing and interacts with cysteine-rich protein 2
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?
additional information
?
-
-
PKG phosphorylates several substrates and interacts, by engaging its N-terminal, with numerous proteins
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?
additional information
?
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cGMP-activated PKGI inhibits TAB1-p38 mitogen-activated protein kinase apoptosis signaling in cardiac myocytes and protects them from ischemia and reperfusion injury, cGMP-activated PKG I does not inhibit MKK3- and MKK6-p38 MAPK signaling, overview
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?
additional information
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PKG-1 is involved in NO-induced cGMP-mediated increase in corpus cavernosum smooth muscle relaxation and penile erection, enzyme disfunction can cause erectile dysfunction, diabetes reduces corpus cavernosum smooth muscle relaxation
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additional information
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PKG phosphorylates several substrates and interacts, by engaging its N-terminal, with numerous proteins
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additional information
?
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PKG phosphorylates several substrates and interacts, by engaging its N-terminal, with numerous proteins
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?
additional information
?
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the enzyme is involved in cGMP-dependent male gametogenesis, i.e. exflagellation, together with Ca2+ release
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additional information
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the enzyme is involved in cGMP-dependent male gametogenesis, i.e. exflagellation, together with Ca2+ release
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additional information
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the enzyme is involved in cGMP-dependent male gametogenesis, i.e. exflagellation, together with Ca2+ release
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additional information
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-
PKG is essential for xanthurenic acid- and zaprinast-induced gametogenesis in Plasmodium falciparum
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?
additional information
?
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global protein phosphorylation pattern of schizonts, overview
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?
additional information
?
-
-
alternative splicing of PKGI in angiotensin-hypertension, mechanism for nitrate tolerance in vascular smooth muscle
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?
additional information
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-
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cyclic GMP-dependent protein kinase regulates CCAAT enhancer-binding protein beta functions through inhibition of glycogen synthase kinase-3
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?
additional information
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PKGII regulates basal level of aldosterone production by zona glomerulosa cells without increasing expression of the steroidogenic acute regulatory protein gene
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?
additional information
?
-
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the enzyme is required for adenosine-induced dilation of intracerebral arterioles and thus in regulation of cerebral blood flow, mechanism
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additional information
?
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the enzyme performs autophosphorylation at serines 110, 114, 117, 126, and 445 and at Thr109 in vitro and in vivo
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?
additional information
?
-
-
the phorbol myristate acetate-stimulated PKC isozyme activates BKCa channels in rat pulmonary arterial smooth muscle via cGMP-dependent protein kinase
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additional information
?
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cGMP-activated PKGI inhibits TAB1-p38 mitogen-activated protein kinase apoptosis signaling in cardiac myocytes and protects them from ischemia and reperfusion injury, cGMP-activated PKG I does not inhibit MKK3- and MKK6-p38 MAPK signaling, overview
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-
?
additional information
?
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PKG I plays a major role in vascular homeostasis by mediating smooth muscle relaxation in response to nitric oxide, regulation of PKG I expression by Rho and Kruppel-like transcription factor-4, RhoA is involved in decreased PKG I levels in vascular smooth muscle cells found in some models of hypertension and vascular injury, overview
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?
additional information
?
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transcriptional regulation by the cgMP/PKG pathway affects the amount of IL-6 expression, cGMP-induced PKG activates the IL-6 promoter involving cis-acting DNA elements and transcription factors, the activation is prevented by actinomycin D, regulation system, overview
-
-
?
additional information
?
-
-
PKG phosphorylates several substrates and interacts, by engaging its N-terminal, with numerous proteins
-
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?
additional information
?
-
-
PKG is involved in the regulation of basal tension and plays a primary role in relaxation induced by nitrovasodilators, whereas PKA may play a minor role
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?
additional information
?
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PKG phosphorylates several substrates and interacts, by engaging its N-terminal, with numerous proteins
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?
additional information
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-
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the enzyme is involved in coccidian parasite motility and invasion and is important in host-parasite interaction
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additional information
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Q8MMP4
the enzyme is involved in gliding motility and cell invasion
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(9S,10R,12R)-2,3,9,10,11,12-hexahydro-10-methoxy-2,9-dimethyl-1-oxo-9,12-epoxy-1H-diindolo [1,2,3-fg:',2',1'-kl]pyrrolo [3,4-i][1,6]benzodiazocine-10-carboxylic acid methyl ester
-
KT-5823, specific PKG inhibitor
(Z)-1-(N-(2-aminoethyl)-N-(2-ammonioethyl)amino)diazen-1-ium-1,2-diolate
-
24 h exposure to 1 mM (Z)-1-(N-(2-aminoethyl)-N-(2-ammonioethyl)amino)diazen-1-ium-1,2-diolate leads to both reduction in cGKI expression and specific activity
1H-[1,2,4]oxadiazolo-[4,3-a]quinoxalin-1-one
-
-
2,2'-(hydroxynitrosohydrazono)-bis-ethanamine
-
24 h incubation with 2,2'-(hydroxynitrosohydrazono)-bis-ethanamine after incubation with cGMP is associated with decreased PKG activity
4-methoxy-3,6-diphenylcyclohexa-3,5-diene-1,2-dione
4-[2-(4-fluorophenyl)-5-(1-methylpiperidin-4-yl)-1H-pyrrol-3-yl]pyridine
4-[2-(4-fluorophenyl)-5-(1-methylpiperidine-4-yl)-1H-pyrrol-3-yl]pyridine
4-[2-(4-fluorophenyl)imidazo[1,2-a]pyridin-3-yl]-N-[4-(4-methylpiperazin-1-yl)phenyl]pyrimidin-2-amine
-
-
4-[2-(4-fluorophenyl)imidazo[1,2-a]pyridin-3-yl]-N-[4-(piperazin-1-yl)phenyl]pyrimidin-2-amine
-
4-[2-(fluorophenyl)-5-(1-methylpiperidine-4-yl)-1H pyrrol-3-yl] pyridine
-
highly specific ATP-competitive inhibitor of PKG
4-[2-(fluorophenyl)-5-(1-methylpiperidine-4-yl)-1H-pyrrol-3-yl]pyridine
4-[2-cyclopropyl-7-[(dimethylamino)methyl]imidazo[1,2-a]pyridin-3-yl]-N-(propan-2-yl)pyrimidin-2-amine
-
-
4-[2-cyclopropyl-7-[(dimethylamino)methyl]imidazo[1,2-a]pyridin-3-yl]-N-(pyridin-2-yl)pyrimidin-2-amine
-
-
4-[2-cyclopropyl-7-[(dimethylamino)methyl]imidazo[1,2-a]pyridin-3-yl]-N-[4-(4-methylpiperazin-1-yl)phenyl]pyrimidin-2-amine
-
-
4-[2-cyclopropyl-7-[(dimethylamino)methyl]imidazo[1,2-a]pyridin-3-yl]-N-[4-(piperazin-1-yl)phenyl]pyrimidin-2-amine
-
-
4-[2-cyclopropyl-7-[(dimethylamino)methyl]imidazo[1,2-a]pyridin-3-yl]pyrimidin-2-amine
-
-
4-[6-[(dimethylamino)methyl]-2-(4-fluorophenyl)imidazo[1,2-a]pyridin-3-yl]pyrimidin-2-amine
-
-
4-[7-[(dimethylamino)methyl]-2-(4-fluorophenyl)-6-methylimidazo[1,2-a]pyridin-3-yl]-N-[4-(piperazin-1-yl)phenyl]pyrimidin-2-amine
-
4-[7-[(dimethylamino)methyl]-2-(4-fluorophenyl)imidazo[1,2-a]pyridin-3-yl]-N-[4-(piperazin-1-yl)phenyl]pyrimidin-2-amine
-
4-[7-[(dimethylamino)methyl]-2-(4-fluorophenyl)imidazo[1,2-a]pyridin-3-yl]pyrimidin-2-amine
-
-
4-[7-[(dimethylamino)methyl]-2-(4-fluorophenyl)imidazo[1,2-a]pyridine-3-yl]pyrimidin-2-amine
4-[7-[(dimethylamino)methyl]-2-[3-(methanesulfonyl)phenyl]imidazo[1,2-a]pyridin-3-yl]pyrimidin-2-amine
-
4-[7-[2-(dimethylamino)ethoxy]-2-(4-fluorophenyl)imidazo[1,2-a]pyridin-3-yl]pyrimidin-2-amine
-
-
4-[7-[2-(dimethylamino)ethyl]-2-(4-fluorophenyl)imidazo[1,2-a]pyridin-3-yl]pyrimidin-2-amine
-
-
4-[8-[(dimethylamino)methyl]-2-(4-fluorophenyl)imidazo[1,2-a]pyridin-3-yl]pyrimidin-2-amine
-
-
5-(piperazine-1-sulfonyl)isoquinoline
-
-
-
6'-methoxy-1,1':4',1''-terphenyl-2,2',5'-triol
6'-methoxy-1,1':4',1''-terphenyl-2,2',5,5'-tetrol
6-anilino-5,8-quinolinedione
-
-
8-(2-[7-nitro-4-benzofurazanyl]aminoethylthio)guanosine-3',5'-cyclic monophosphate
-
the compound significantly reduces the kinase activity of the enzyme and is the most potent inhibitor
-
8-(4-chlorophenylthio)-beta-phenyl-1,N2-ethenoguanosine-3'5'-cyclic monophophorothioate, Rp isomer
-
-
-
8-(4-chlorophenylthio)-guanosine-3'5'-cyclic monophophosphate
-
-
-
8-(4-chlorophenylthio)guanosine 3',5'-cyclic monophosphate
-
-
8-(4-chlorophenylthio)guanosine 3',5'-cyclic monophosphorothioate Rp-isomer
-
-
8-(4-chlorophenylthio)guanosine-3',5'-cyclic monophosphorothioate
-
the compound significantly reduces the kinase activity of the enzyme
-
all-D-YGRKKRRQRRRPPLRKKKKKH
angiotensin
-
causes a decrease in expression of isozyme cGKIalpha, and an increase in expression of isozyme cGKIbeta
beta-phenyl-1,N2-etheno-8-bromoguanosine-3',5'-cyclic monophosphorothioate
-
-
D-glucose
-
high levels reduce enzyme activity in vivo leading to increased thrombospondin 1-dependent activation of transforming growth factor-beta, and increased TGF-beta-dependent expression of fibronectin and collagene type IV
N-(3-[3-(2-aminopyrimidin-4-yl)-7-[(dimethylamino)methyl]imidazo[1,2-a]pyridin-2-yl]phenyl)methanesulfonamide
-
N-(5-[3-(2-aminopyrimidin-4-yl)-7-[(dimethylamino)methyl]-6-methylimidazo[1,2-a]pyridin-2-yl]-2-fluorophenyl)methanesulfonamide
-
N-(5-[3-(2-aminopyrimidin-4-yl)-7-[(dimethylamino)methyl]imidazo[1,2-a]pyridin-2-yl]-2-fluorophenyl)methanesulfonamide
-
N-(cyclopropylmethyl)-4-[7-[(dimethylamino)methyl]-2-[3-(methanesulfonyl)phenyl]imidazo[1,2-a]pyridin-3-yl]pyrimidin-2-amine
-
N-[2-(methylamino)ethyl]-5-isoquinolinesulfonamide
-
-
N-[5-(3-[2-[(cyclopropylmethyl)amino]pyrimidin-4-yl]-7-[(dimethylamino)methyl]-6-methylimidazo[1,2-a]pyridin-2-yl)-2-fluorophenyl]methanesulfonamide
-
N2-[2-(4-fluorophenyl)-3-[2-(methylamino)pyrimidin-4-yl]imidazo[1,2-a]pyridin-7-yl]-N1,N1-dimethylethane-1,2-diamine
-
-
N2-[3-(2-aminopyrimidin-4-yl)-2-(4-fluorophenyl)imidazo[1,2-a]pyridin-7-yl]-N1,N1-dimethylethane-1,2-diamine
-
-
N3-[3-(2-aminopyrimidin-4-yl)-2-(4-fluorophenyl)imidazo[1,2-a]pyridin-6-yl]-N1,N1-dimethylpropane-1,3-diamine
-
-
nitroglycerine
-
24 h incubation with nitroglycerine after incubation with cGMP is associated with decreased PKG activity, PKG mRNA and protein are downregulated by a 24 h incubation with nitroglycerine at 0.01 mM but not at 0.0001 mM
pyrrole 4-[2-(4-fluorophenyl)-5-(1-methylpiperidine-4-yl)-1H pyrrol-3-yl] pyridine
-
inhibits native and recombinant enzyme, shows antiparasitic activity being active against Plasmodium falciparum blood cell stages cultured in vitro, IC50 for the native enzyme is 8.35 nM, and for the recombinant FLAG-tagged enzyme 3.48 nM
regulatory subunit of photoreceptor cGMP phosphodiesterase
-
inhibits PKGIalpha, the N-terminal 61 amino acids are important containing a cationic region
-
retro-inverso-all-D-YGRKKRRQRRRPPLRKKKKKH
Rp-8-Br-cGMP
-
in vivo inhibition in leukemia cells causes reduced agonist-stimulated beta-hexosaminidase release and abolishes vesicular fusion with the plasma membrane
Rp-8-p-CPT-cGMP
-
i.e. Rp-8-(4-chlorophenylthio)guanosine 3',5'-cyclic monophosphate
Rp-8-pCTP-cGMPS
-
selective for PKG
TTYDFIASGRTGRRNAIHD-NH2
-
-
4-methoxy-3,6-diphenylcyclohexa-3,5-diene-1,2-dione
-
isolated from a microbial extract of a Phoma sp.
4-methoxy-3,6-diphenylcyclohexa-3,5-diene-1,2-dione
-
isolated from a microbial extract of a Phoma sp.
4-[2-(4-fluorophenyl)-5-(1-methylpiperidin-4-yl)-1H-pyrrol-3-yl]pyridine
-
a synthetic compound
4-[2-(4-fluorophenyl)-5-(1-methylpiperidin-4-yl)-1H-pyrrol-3-yl]pyridine
-
a synthetic compound
4-[2-(4-fluorophenyl)-5-(1-methylpiperidine-4-yl)-1H-pyrrol-3-yl]pyridine
-
inhibits downstream of calcium-dependent events, inhibition is not reversible by calcium ionophores or ethanol, inhibits uracil uptake, blocks the attachment of the sporozoite to the host cells and inhibits parasite invasion and gliding motility, inhibits the secretion of micronemal adhesins MIC1 and MIC2 by the parasite, no inhibition of mutants T770M and T770Q
4-[2-(4-fluorophenyl)-5-(1-methylpiperidine-4-yl)-1H-pyrrol-3-yl]pyridine
-
inhibits downstream of calcium-dependent events, inhibition is not reversible by calcium ionophores or ethanol, inhibits uracil uptake, blocks the attachment of the tachyzoite to the host cells and inhibits parasite invasion and gliding motility, inhibits the secretion of micronemal adhesin MIC2 by the parasite, no inhibition of mutants T761M and T761Q
4-[2-(4-fluorophenyl)imidazo[1,2-a]pyridin-3-yl]-N-[4-(piperazin-1-yl)phenyl]pyrimidin-2-amine
-
-
-
4-[2-(4-fluorophenyl)imidazo[1,2-a]pyridin-3-yl]-N-[4-(piperazin-1-yl)phenyl]pyrimidin-2-amine
-
-
-
4-[2-(4-fluorophenyl)imidazo[1,2-a]pyridin-3-yl]-N-[4-(piperazin-1-yl)phenyl]pyrimidin-2-amine
-
-
4-[2-(4-fluorophenyl)imidazo[1,2-a]pyridin-3-yl]-N-[4-(piperazin-1-yl)phenyl]pyrimidin-2-amine
-
-
4-[2-(fluorophenyl)-5-(1-methylpiperidine-4-yl)-1H-pyrrol-3-yl]pyridine
inhibitor of apicomplexan parasite enzyme, IC50 is 1 nM for the enzyme of Eimeria tenella, mechanism
4-[2-(fluorophenyl)-5-(1-methylpiperidine-4-yl)-1H-pyrrol-3-yl]pyridine
Q8MMP4
inhibitor of apicomplexan parasite enzyme, mechanism
4-[7-[(dimethylamino)methyl]-2-(4-fluorophenyl)-6-methylimidazo[1,2-a]pyridin-3-yl]-N-[4-(piperazin-1-yl)phenyl]pyrimidin-2-amine
-
-
-
4-[7-[(dimethylamino)methyl]-2-(4-fluorophenyl)-6-methylimidazo[1,2-a]pyridin-3-yl]-N-[4-(piperazin-1-yl)phenyl]pyrimidin-2-amine
-
-
-
4-[7-[(dimethylamino)methyl]-2-(4-fluorophenyl)-6-methylimidazo[1,2-a]pyridin-3-yl]-N-[4-(piperazin-1-yl)phenyl]pyrimidin-2-amine
-
-
4-[7-[(dimethylamino)methyl]-2-(4-fluorophenyl)-6-methylimidazo[1,2-a]pyridin-3-yl]-N-[4-(piperazin-1-yl)phenyl]pyrimidin-2-amine
-
-
4-[7-[(dimethylamino)methyl]-2-(4-fluorophenyl)imidazo[1,2-a]pyridin-3-yl]-N-[4-(piperazin-1-yl)phenyl]pyrimidin-2-amine
-
-
-
4-[7-[(dimethylamino)methyl]-2-(4-fluorophenyl)imidazo[1,2-a]pyridin-3-yl]-N-[4-(piperazin-1-yl)phenyl]pyrimidin-2-amine
-
-
-
4-[7-[(dimethylamino)methyl]-2-(4-fluorophenyl)imidazo[1,2-a]pyridin-3-yl]-N-[4-(piperazin-1-yl)phenyl]pyrimidin-2-amine
-
-
4-[7-[(dimethylamino)methyl]-2-(4-fluorophenyl)imidazo[1,2-a]pyridin-3-yl]-N-[4-(piperazin-1-yl)phenyl]pyrimidin-2-amine
-
-
4-[7-[(dimethylamino)methyl]-2-(4-fluorophenyl)imidazo[1,2-a]pyridine-3-yl]pyrimidin-2-amine
-
-
4-[7-[(dimethylamino)methyl]-2-(4-fluorophenyl)imidazo[1,2-a]pyridine-3-yl]pyrimidin-2-amine
-
-
4-[7-[(dimethylamino)methyl]-2-(4-fluorophenyl)imidazo[1,2-a]pyridine-3-yl]pyrimidin-2-amine
-
-
4-[7-[(dimethylamino)methyl]-2-(4-fluorophenyl)imidazo[1,2-a]pyridine-3-yl]pyrimidin-2-amine
-
4-[7-[(dimethylamino)methyl]-2-(4-fluorophenyl)imidazo[1,2-a]pyridine-3-yl]pyrimidin-2-amine
-
4-[7-[(dimethylamino)methyl]-2-[3-(methanesulfonyl)phenyl]imidazo[1,2-a]pyridin-3-yl]pyrimidin-2-amine
-
-
-
4-[7-[(dimethylamino)methyl]-2-[3-(methanesulfonyl)phenyl]imidazo[1,2-a]pyridin-3-yl]pyrimidin-2-amine
-
-
-
4-[7-[(dimethylamino)methyl]-2-[3-(methanesulfonyl)phenyl]imidazo[1,2-a]pyridin-3-yl]pyrimidin-2-amine
-
-
4-[7-[(dimethylamino)methyl]-2-[3-(methanesulfonyl)phenyl]imidazo[1,2-a]pyridin-3-yl]pyrimidin-2-amine
-
-
6'-methoxy-1,1':4',1''-terphenyl-2,2',5'-triol
-
isolated from a microbial extract of a Phoma sp.
6'-methoxy-1,1':4',1''-terphenyl-2,2',5'-triol
-
isolated from a microbial extract of a Phoma sp.
6'-methoxy-1,1':4',1''-terphenyl-2,2',5,5'-tetrol
-
isolated from a microbial extract of a Phoma sp.
6'-methoxy-1,1':4',1''-terphenyl-2,2',5,5'-tetrol
-
isolated from a microbial extract of a Phoma sp.
all-D-YGRKKRRQRRRPPLRKKKKKH
-
-
all-D-YGRKKRRQRRRPPLRKKKKKH
-
-
all-D-YGRKKRRQRRRPPLRKKKKKH
-
-
DT-2 peptide
-
a HIV tat peptide sequence, blocks type 1 PKG
DT3
-
-
KT-5823
-
-
KT5823
-
-
KT5823
-
a specific PKG inhibitor, PKG inhibition induces rapid thermotolerance of neural circuitry
KT5823
-
staurosporine analogue, inhibits in vitro by selective blockage of ATP binding
KT5823
-
specific PKG inhibitor
KT5823
-
staurosporine analogue, inhibits in vitro by selective blockage of ATP binding
KT5823
-
selective inhibitor of isoform PKG-I
KT5823
-
i.e. (8R,9S,11S)-(-)-9-methoxy-carbamyl-8-methyl-2,3,9,10-tetrahydro-8,11-epoxy-1H,8H-2,7b,11a-trizadizobenzo9(a,g)cycloocta(c,d,e)-trinden-1-one, selective PKG inhibitor
KT5823
PKG inhibitor; PKG inhibitor
KT5823
-
i.e. (8R,9S,11S)-(-)-9-methoxy-carbamyl-8-methyl-2,3,9,10-tetrahydro-8,11-epoxy-1H,8H,11H-2,7b,11a-trizadibenzo-(a,g)-cycloocta-(c,d,e)-trinden-1-one, potent and highly specific inhibitor
KT5823
-
specific antagonist
KT5823
-
specific for PKG
KT5823
-
in vivo inhibition in leukemia cells causes reduced agonist-stimulated beta-hexosaminidase release and abolishes vesicular fusion with the plasma membrane
KT5823
-
effect of KT5823 is abolished in the presence of the nonselective cyclic nucleotide PDE inhibitor 3-isobutyl-1-methylxantine or the selective cGMP-PDE5 inhibitor sildenafil
KT5926
-
N-(3-[3-(2-aminopyrimidin-4-yl)-7-[(dimethylamino)methyl]imidazo[1,2-a]pyridin-2-yl]phenyl)methanesulfonamide
-
-
-
N-(3-[3-(2-aminopyrimidin-4-yl)-7-[(dimethylamino)methyl]imidazo[1,2-a]pyridin-2-yl]phenyl)methanesulfonamide
-
-
-
N-(3-[3-(2-aminopyrimidin-4-yl)-7-[(dimethylamino)methyl]imidazo[1,2-a]pyridin-2-yl]phenyl)methanesulfonamide
-
-
N-(3-[3-(2-aminopyrimidin-4-yl)-7-[(dimethylamino)methyl]imidazo[1,2-a]pyridin-2-yl]phenyl)methanesulfonamide
-
-
N-(5-[3-(2-aminopyrimidin-4-yl)-7-[(dimethylamino)methyl]-6-methylimidazo[1,2-a]pyridin-2-yl]-2-fluorophenyl)methanesulfonamide
-
-
-
N-(5-[3-(2-aminopyrimidin-4-yl)-7-[(dimethylamino)methyl]-6-methylimidazo[1,2-a]pyridin-2-yl]-2-fluorophenyl)methanesulfonamide
-
-
-
N-(5-[3-(2-aminopyrimidin-4-yl)-7-[(dimethylamino)methyl]-6-methylimidazo[1,2-a]pyridin-2-yl]-2-fluorophenyl)methanesulfonamide
-
-
N-(5-[3-(2-aminopyrimidin-4-yl)-7-[(dimethylamino)methyl]-6-methylimidazo[1,2-a]pyridin-2-yl]-2-fluorophenyl)methanesulfonamide
-
-
N-(5-[3-(2-aminopyrimidin-4-yl)-7-[(dimethylamino)methyl]imidazo[1,2-a]pyridin-2-yl]-2-fluorophenyl)methanesulfonamide
-
-
-
N-(5-[3-(2-aminopyrimidin-4-yl)-7-[(dimethylamino)methyl]imidazo[1,2-a]pyridin-2-yl]-2-fluorophenyl)methanesulfonamide
-
-
-
N-(5-[3-(2-aminopyrimidin-4-yl)-7-[(dimethylamino)methyl]imidazo[1,2-a]pyridin-2-yl]-2-fluorophenyl)methanesulfonamide
-
-
N-(5-[3-(2-aminopyrimidin-4-yl)-7-[(dimethylamino)methyl]imidazo[1,2-a]pyridin-2-yl]-2-fluorophenyl)methanesulfonamide
-
-
N-(cyclopropylmethyl)-4-[7-[(dimethylamino)methyl]-2-[3-(methanesulfonyl)phenyl]imidazo[1,2-a]pyridin-3-yl]pyrimidin-2-amine
-
-
-
N-(cyclopropylmethyl)-4-[7-[(dimethylamino)methyl]-2-[3-(methanesulfonyl)phenyl]imidazo[1,2-a]pyridin-3-yl]pyrimidin-2-amine
-
-
-
N-(cyclopropylmethyl)-4-[7-[(dimethylamino)methyl]-2-[3-(methanesulfonyl)phenyl]imidazo[1,2-a]pyridin-3-yl]pyrimidin-2-amine
-
-
N-(cyclopropylmethyl)-4-[7-[(dimethylamino)methyl]-2-[3-(methanesulfonyl)phenyl]imidazo[1,2-a]pyridin-3-yl]pyrimidin-2-amine
-
-
N-[5-(3-[2-[(cyclopropylmethyl)amino]pyrimidin-4-yl]-7-[(dimethylamino)methyl]-6-methylimidazo[1,2-a]pyridin-2-yl)-2-fluorophenyl]methanesulfonamide
-
most potent inhibitor
-
N-[5-(3-[2-[(cyclopropylmethyl)amino]pyrimidin-4-yl]-7-[(dimethylamino)methyl]-6-methylimidazo[1,2-a]pyridin-2-yl)-2-fluorophenyl]methanesulfonamide
-
most potent inhibitor
-
N-[5-(3-[2-[(cyclopropylmethyl)amino]pyrimidin-4-yl]-7-[(dimethylamino)methyl]-6-methylimidazo[1,2-a]pyridin-2-yl)-2-fluorophenyl]methanesulfonamide
most potent inhibitor
-
N-[5-(3-[2-[(cyclopropylmethyl)amino]pyrimidin-4-yl]-7-[(dimethylamino)methyl]-6-methylimidazo[1,2-a]pyridin-2-yl)-2-fluorophenyl]methanesulfonamide
most potent inhibitor
-
retro-inverso-all-D-YGRKKRRQRRRPPLRKKKKKH
-
-
retro-inverso-all-D-YGRKKRRQRRRPPLRKKKKKH
-
-
retro-inverso-all-D-YGRKKRRQRRRPPLRKKKKKH
-
-
Rp-8-Br-pCPT-cGMPS
-
-
Rp-8-Br-pCPT-cGMPS
-
i.e. Rp-8-bromo-(4-chlorophenylthio)guanosine 3',5'-cyclic monophosphate
Rp-8-Br-PET-cGMPS
-
beta-phenyl-1,N2-etheno-8-bromoguanosine-3',5'-cyclic monophosphorothioate
Rp-8-Br-PET-cGMPS
-
PKG-I inhibition leads to abolished induction of p38 by thrombin
Rp-8-Br-PET-cGMPS
-
beta-phenyl-1,N2-etheno-8-bromoguanosine-3',5'-cyclic monophosphorothioate
Rp-8-Br-PET-cGMPS
-
the PKG inhibitor has no effect in vivo on the basal tension of vessels treated with nitro-L-arginine, nitro-L-arginine plus indomethacin, or of vessels denuded of the endothelium, overview
Rp-8-pCPT-cGMP
-
i.e. 8-(4-chlorophenylthio)guanosine-3',5'-cyclic monophosphorothionate Rp isomer, inhibits DG2P1 and DG2P2 at 0.01 and 0.1 mM, respectively
Rp-8-pCPT-cGMP
-
Rp-i.e. 8-(4-chlorophenylthio)guanosine 3',5'-cyclic monophosphate
Rp-8-pCPT-cGMP
-
i.e. Rp-8-(4-chlorophenylthio)guanosine 3',5'-cyclic monophosphate, cGKI inhibitor, reverses the NO effects
Rp-8-pCPT-cGMPS
-
-
Rp-8-pCPT-cGMPS
-
PKG inhibitor
Rp-8-pCPT-cGMPS
a cGMP analogue
Rp-pCPT-cGMPS
-
-
staurosporine
-
terferol
-
isolated from a microbial extract of a Phoma sp.
terferol
-
isolated from a microbial extract of a Phoma sp.
YGRKKRRQRRRPPLRKKKKKH
-
-
YGRKKRRQRRRPPLRKKKKKH
-
-
YGRKKRRQRRRPPLRKKKKKH
-
-
YGRKKRRQRRRPPLRKKKKKH
-
-
additional information
the enzyme possesses an N-terminal autoinhibitory sequence
-
additional information
-
the enzyme possesses an N-terminal autoinhibitory sequence
-
additional information
-
the enzyme possesses an N-terminal autoinhibitory sequence
-
additional information
-
the enzyme possesses an N-terminal autoinhibitory sequence
-
additional information
-
the enzyme possesses an N-terminal autoinhibitory sequence
-
additional information
the enzyme possesses an N-terminal autoinhibitory sequence
-
additional information
the enzyme possesses an N-terminal autoinhibitory sequence
-
additional information
the enzyme possesses an N-terminal autoinhibitory sequence
-
additional information
the enzyme possesses an N-terminal autoinhibitory sequence ERKVQKAIKQQE
-
additional information
-
PKG-I inhibition leads to abolished induction of p38 by thrombin
-
additional information
-
the enzyme is inactivated by expression of a dominant negative mutant type 1alpha PKG construct
-
additional information
-
inhibition by DT-2 fusion peptide of in vitro peptide inhibitor W45 and the membrane translocation signal sequences from HIV tyrosine aminotransferase protein, and DT-3 fusion peptide of W45 and the Drosophila antennapedia homeodomain
-
additional information
-
the enzyme possesses an N-terminal autoinhibitory sequence
-
additional information
-
inhibition of PKG affects platelet secretion, platelet aggregation, and Ca2+ mobilization
-
additional information
-
PKGI contains autoinhibitory subdomains in the regulatory domains and two allosteric cGMP-binding sites of isozymes alpha and beta
-
additional information
-
the enzyme is regulated via negative feedback
-
additional information
the R-diastereomer of the phosphorothioate analog of cGMP, Rp-cGMPS, inhibits enzyme isoform PKG I by stabilizing the inactive conformation of cyclic nucleotide-binding domain
-
additional information
-
the Rp-isomer of 8-(4-chlorophenylthio)guanosine-3'5'-cyclic monophophorothioate does not inhibit the activity of the enzyme
-
additional information
the enzyme possesses an N-terminal autoinhibitory sequence
-
additional information
-
cGK II contains an autoinhibitory region
-
additional information
-
enzyme activity is reduced in diabetic rabbits
-
additional information
-
no inhibition by myristoylated PKI14-22 amide
-
additional information
the enzyme possesses an N-terminal autoinhibitory sequence; the enzyme possesses an N-terminal autoinhibitory sequence ERNKKKAIFSND
-
additional information
the enzyme possesses an N-terminal autoinhibitory sequence; the enzyme possesses an N-terminal autoinhibitory sequence ERNKKKAIFSND
-
additional information
-
the enzyme possesses an N-terminal autoinhibitory sequence ERNKKKAIFSND
-
additional information
-
the enzyme possesses an N-terminal autoinhibitory sequence
-
additional information
-
PKGII inhibition inhibits aldosterone production
-
additional information
-
Rho and Krueppel-like transcription factor-4 KLF4, a bound nuclear protein, suppress PKG I expression requiring Sp1 consensus sequences in the PKG I promoter, suppression in a in a cell density-dependent manner
-
additional information
-
no inhibition by the PKA-specific inhibitor myristoylated PKI
-
additional information
-
superoxide and 8-bromo-cAMP have no effect on PKG activity
-
additional information
-
the enzyme possesses an N-terminal autoinhibitory sequence
-
additional information
Q8MMP4
the enzyme possesses an N-terminal autoinhibitory sequence
-
Please wait a moment until the data is sorted. This message will disappear when the data is sorted.
1,4:3,6-dianhydro-D-glucitol 5-nitrate
-
isosorbide mononitrate
-
20 kDa heat shock protein
-
i.e. Hsp20, involved in cGKI-induced smooth muscle relaxation, probably via the actin binding sequence
-
8-(4-chlorophenylthio) guanosine-3',5'-cyclic monophosphate
-
-
8-(4-chlorophenylthio)-3',5'-cyclic GMP
-
-
8-(4-chlorophenylthio)guanosine 3',5'-cyclic monophosphate
-
-
8-(4-chlorophenylthio)guanosine-3',5'-cyclic monophosphate
-
-
8-APT-cGMP
-
cGKIalpha-selective activator
8-NBD-cGMP
i.e. 8-[[2-[(7-nitro-4-benzofurazanyl)amino]ethyl]thio]guanosine-3',5'-cyclic monophosphate, poor, non-cooperative binding
adenosine
-
adenosine-induced vasodilation in cerebral microvessesls involves cGMP and cGMP-dependent protein kinase
angiotensin
-
causes an increase in expression of isozyme cGKIbeta, and a decrease in expression of isozyme cGKIalpha
atrial natriuretic peptide
-
0.00001-0.01 mM
-
beta-phenyl-1,N2-ethenoguanosine-3',5'-cyclic monophosphate
-
-
-
calcium/calmodulin-dependent kinase II
-
mediates NO-elicited PKG activation
-
cAMP
-
crossactivation at high levels in vivo
dibutyryl-cGMP
-
0.001-0.1 mM
formyl-methionyl-leucyl-phenylalanine
-
-
forskolin
-
crossactivation at high levels above 0.001 mM in vivo
FoxO1a
-
directly activates enzyme expression binding to DNA in skeletal muscle
-
isoproterenol
-
crossactivation at high levels above 0.001 mM in vivo
lipopolysaccharides
-
induces enzyme expression and activates the enzyme
-
N2,2'-O-dibutyryl-cGMP
-
a membrane-permeable cGMP analogue, activates cGKI
S-nitroso-N-acetyl-DL-penicillamine
-
-
Sp-8-pCPT-cGMPS
-
cyclic guanosine monophosphate-dependent protein kinase activator, selective for PKG
Sp-8-pCPT-PET-cGMPS
-
the compound significantly increases protein phosphorylation by 250%
-
Vasoactive intestinal peptide
-
i.e. VIP
8-Br-cGMP
-
-
8-Br-cGMP
-
activation of cGKIalpha and cGKII, specificity overview
8-Br-cGMP
-
selective for PKG
8-Br-PET-cGMP
-
activation of cGKIalpha and cGKII, specificity overview
8-Br-PET-cGMP
-
highly specific activator of both the A and B isoforms of cGMP-dependent protein kinase I
8-bromo-cGMP
-
PKG activator 8-bromo-cGMP abolishes thermoprotective effect of a prior heat shock
8-bromo-cGMP
-
activation of cGKII by 8-bromo-cGMP enhances the surface expression of GluA1, whereas its inhibition or suppression effectively diminishes the expression of this protein at the cell surface
8-pCPT-CGMP
-
i.e. 8-(4-chlorophenylthio)guanosine 3',5'-cyclic monophosphate
8-pCPT-CGMP
-
i.e. 8-(4-chlorophenylthio)guanosine 3',5'-cyclic monophosphate, activation of cGKIalpha and cGKII, specificity overview
8-pCPT-CGMP
-
i.e. i.e. 8-(4-chlorophenylthio)guanosine 3',5'-cyclic monophosphate, cGMP analogue, membrane-permeable
8-pCPT-CGMP
-
i.e. 8-(4-chlorophenylthio)guanosine 3',5'-cyclic monophosphate
8-pCPT-CGMP
-
i.e. 8-(4-chlorophenylthio)guanosine 3',5'-cyclic monophosphate, 358% activation, inhibitor KT5823 abolishes the activating effect
8-pCPT-CGMP
-
i.e. 8-(4-chlorophenylthio)guanosine 3',5'-cyclic monophosphate
Bay412272
-
YC1 analogue, stimulates the enzyme in a NO-dependent manner, inhibition of phosphodiesterase 5
Bay412272
-
YC1 analogue, stimulates the enzyme in a NO-dependent manner, inhibition of phosphodiesterase 5
cGMP
-
cGMP
-
molecular mechanism and thermodynamics
cGMP
large conformational changes accompany cGMP binding to the enzyme. A distinct and segregated architecture with an extended central helix separates the two cGMPbinding domains. Additionally, a helical domain (switch helix) promotes the formation of a hydrophobic interface between protomers
cGMP
-
PKG-I is activated by the NO/sGC/cGMP system
cGMP
-
stimulates DG2P1 and DG2P2, and DG1, the latter maximally at 20 mM
cGMP
highly activating, binding site analysis, cooperative binding
cGMP
-
-
661575, 661813, 662170, 662277, 671256, 672779, 672785, 673013, 676003, 701630, 702471, 703570, 762071
cGMP
-
activates native and recombinant enzyme
cGMP
-
highly dependent on, about 10fold activation, binding and activation mechanisms for wild-type and mutant PKG-Ibeta, modeling, the enzyme elongates upon cGMP binding
cGMP
-
required by the full length enzyme for activity, the activity of the recombinant catalytic domain is independent of cGMP
cGMP
-
two allosteric binding sites in the regulatory domains in PKGI isozymes, structure and mechanism, enzyme elongation by cGMP binding ehich induces conformational changes, overview
cGMP
-
PKG-I is activated by the NO/sGC/cGMP system
cGMP
activation constant (Ka) of 537 nM
cGMP
-
cGK I and cGK II contain a high and a low affinity binding site for cGMP with opposite orientation in cGK II compared to cGK I
cGMP
-
activates native and recombinant enzyme
cGMP
-
PKG-I is activated by the NO/sGC/cGMP system
cGMP
-
PKG-I is activated by the NO/sGC/cGMP system
cGMP
-
PKG-I is activated by the NO/sGC/cGMP system
cGMP
binding site analysis, positive cooperativity at low concentration
cGMP
-
binding site analysis, positive cooperativity at low concentration
cGMP
-
cooperative kinetics of stimulation
cGMP
-
activates both PKGI and PKGII
cGMP
-
activates native and recombinant enzyme, the activation of recombinant cGKII is reduced because the enzyme already partially phosphorylated
cGMP
-
level is increased by NO and glutamate
cGMP
-
cGMP-dependent activation of GKII depends on NO produced by nitric oxide synthase upon NMDA receptor activation
cGMP
-
PKG-I is activated by the NO/sGC/cGMP system
cGMP
-
PKG-I is activated by the NO/sGC/cGMP system
cGMP
Q8MMP4
highly activating, binding site analysis
nitric oxide
-
-
NO
-
-
NO
-
NO stimulates PKGI in vascular smooth umscle cells contributing to cytoskelatl kinetics and phenotype, overview
PET-cGMP
-
activation of cGKIalpha and cGKII, specificity overview
sodium nitroprusside
-
i.e. SNP, selective activator of PKG, 414% activation, inhibitor KT5823 abolishes the activating effect
sodium nitroprusside
-
i.e. SNP, selective for PKG
YC1
-
i.e. 3-(5'-hydroxymethyl-2'-furyl)-1-benzylindazole, hem-dependent activation of cGK, inhibition of phosphodiesterase 5
YC1
-
i.e. 3-(5'-hydroxymethyl-2'-furyl)-1-benzylindazole, hem-dependent activation of cGK, inhibition of phosphodiesterase 5
additional information
aminoterminal dimerization site of cGMP-dependent protein kinase and the autophosphorylation site, present in this part, control not only the activation of the enzyme but also the cooperative binding characteristics of the intact enzyme
-
additional information
-
cGKI activity is induced by NO via increased cGMP production
-
additional information
-
cGKII is upregulated by aldosterone inducation e.g. via low salt diet, NO induces cGMP production and thus increases enzyme activity, cGK is also activates via increased cGMP level by inhibition of the phosphodiesterase 5 by sildenafil, vardenafil, and taladafil, or by inhibition of Ca2+/calmodulin-specific cGMP-dependent phosphodiesterase 1
-
additional information
-
enzyme is induced by NO via cGMP
-
additional information
-
NO activates the enzyme via increased cGMP level leading to vascular relaxation
-
additional information
-
NO induces the enzyme via increased cGMP production
-
additional information
-
NO, from NO donor sodium nitroprusside, induces cGMP production and thus increases enzyme activity
-
additional information
-
mechanical stress also induces the enzyme, e.g. in lung epithelial cells, umbilical vein endothelial cells, and osteoblasts
-
additional information
-
the activity of transient receptor potential channel 6 channels is markedly suppressed by PKG activation
-
additional information
-
isozymes cGK I and cGK II exhibit different affinity for cGMP analogues, overview
-
additional information
-
NO induces cGMP production which activates the enzyme
-
additional information
-
cGKII is upregulated by aldosterone inducation e.g. via low salt diet, NO induces cGMP production and thus increases enzyme activity, cGK is also activates via increased cGMP level by inhibition of the phosphodiesterase 5 by sildenafil, vardenafil, and taladafil, or by inhibition of Ca2+/calmodulin-specific cGMP-dependent phosphodiesterase 1
-
additional information
-
NO induces cGMP production and thus increases enzyme activity
-
additional information
-
NO, from NO donor sodium nitroprusside, induces cGMP production and thus increases enzyme activity
-
additional information
-
the enzyme mediates NO antiatherogenic and proatherogenic effects
-
additional information
cGKI can be activated by natriuretic peptide receptor-B dependent cGMP production
-
additional information
-
cGKI can be activated by natriuretic peptide receptor-B dependent cGMP production
-
additional information
-
high glucose levels induce NO-induced stimulation of cGMP production and increase PKG-1 activity
-
additional information
-
glutamate induced NO, and increased NO release from sodium nitroprusside and S-nitroso-N-acetylpenicillamine increase cGMP level which increases PKG activity, overview
-
additional information
-
NO activates the enzyme through elevation of cGMP concentration, reduced in hypertensive rats due to a shift in relation of cGKIalpha to cGKIbeta
-
additional information
-
Rac1 stimulates PKG I expression
-
additional information
-
the activity of transient receptor potential channel 6 channels is markedly suppressed by PKG activation
-
Please wait a moment until the data is sorted. This message will disappear when the data is sorted.
Please wait a moment until the data is sorted. This message will disappear when the data is sorted.
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0.0009
4-methoxy-3,6-diphenylcyclohexa-3,5-diene-1,2-dione
Eimeria tenella
-
-
0.000001 - 0.00021
4-[2-(4-fluorophenyl)-5-(1-methylpiperidin-4-yl)-1H-pyrrol-3-yl]pyridine
0.00000171 - 0.001713
4-[2-(4-fluorophenyl)imidazo[1,2-a]pyridin-3-yl]-N-[4-(piperazin-1-yl)phenyl]pyrimidin-2-amine
-
0.00000155 - 0.0178
4-[2-(fluorophenyl)-5-(1-methylpiperidine-4-yl)-1H pyrrol-3-yl] pyridine
0.000001
4-[2-(fluorophenyl)-5-(1-methylpiperidine-4-yl)-1H-pyrrol-3-yl]pyridine
Eimeria tenella
inhibitor of apicomplexan parasite enzyme, IC50 is 1 nM for the enzyme of Eimeria tenella, mechanism
0.00000045 - 0.000231
4-[7-[(dimethylamino)methyl]-2-(4-fluorophenyl)-6-methylimidazo[1,2-a]pyridin-3-yl]-N-[4-(piperazin-1-yl)phenyl]pyrimidin-2-amine
-
0.00000079 - 0.000842
4-[7-[(dimethylamino)methyl]-2-(4-fluorophenyl)imidazo[1,2-a]pyridin-3-yl]-N-[4-(piperazin-1-yl)phenyl]pyrimidin-2-amine
-
0.0000031 - 0.0084
4-[7-[(dimethylamino)methyl]-2-(4-fluorophenyl)imidazo[1,2-a]pyridine-3-yl]pyrimidin-2-amine
0.00000088 - 0.1
4-[7-[(dimethylamino)methyl]-2-[3-(methanesulfonyl)phenyl]imidazo[1,2-a]pyridin-3-yl]pyrimidin-2-amine
-
0.0052 - 0.0104
6'-methoxy-1,1':4',1''-terphenyl-2,2',5'-triol
0.0058 - 0.0095
6'-methoxy-1,1':4',1''-terphenyl-2,2',5,5'-tetrol
0.000012
all-D-YGRKKRRQRRRPPLRKKKKKH
Homo sapiens
-
-
0.00023
KT5823
Homo sapiens
-
-
0.00000434 - 0.1
N-(3-[3-(2-aminopyrimidin-4-yl)-7-[(dimethylamino)methyl]imidazo[1,2-a]pyridin-2-yl]phenyl)methanesulfonamide
-
0.00000119 - 0.1
N-(5-[3-(2-aminopyrimidin-4-yl)-7-[(dimethylamino)methyl]-6-methylimidazo[1,2-a]pyridin-2-yl]-2-fluorophenyl)methanesulfonamide
-
0.00000079 - 0.0737
N-(5-[3-(2-aminopyrimidin-4-yl)-7-[(dimethylamino)methyl]imidazo[1,2-a]pyridin-2-yl]-2-fluorophenyl)methanesulfonamide
-
0.00000013 - 0.0525
N-(cyclopropylmethyl)-4-[7-[(dimethylamino)methyl]-2-[3-(methanesulfonyl)phenyl]imidazo[1,2-a]pyridin-3-yl]pyrimidin-2-amine
-
0.00000016 - 0.02954
N-[5-(3-[2-[(cyclopropylmethyl)amino]pyrimidin-4-yl]-7-[(dimethylamino)methyl]-6-methylimidazo[1,2-a]pyridin-2-yl)-2-fluorophenyl]methanesulfonamide
-
0.00000348 - 0.00000835
pyrrole 4-[2-(4-fluorophenyl)-5-(1-methylpiperidine-4-yl)-1H pyrrol-3-yl] pyridine
0.000054
retro-inverso-all-D-YGRKKRRQRRRPPLRKKKKKH
Homo sapiens
-
-
0.000332
YGRKKRRQRRRPPLRKKKKKH
Homo sapiens
-
-
0.000001
4-[2-(4-fluorophenyl)-5-(1-methylpiperidin-4-yl)-1H-pyrrol-3-yl]pyridine
Eimeria tenella
-
-
0.00021
4-[2-(4-fluorophenyl)-5-(1-methylpiperidin-4-yl)-1H-pyrrol-3-yl]pyridine
Toxoplasma gondii
-
-
0.00000171
4-[2-(4-fluorophenyl)imidazo[1,2-a]pyridin-3-yl]-N-[4-(piperazin-1-yl)phenyl]pyrimidin-2-amine
Plasmodium falciparum
wild type enzyme, at pH 7.4 and 25°C
-
0.001713
4-[2-(4-fluorophenyl)imidazo[1,2-a]pyridin-3-yl]-N-[4-(piperazin-1-yl)phenyl]pyrimidin-2-amine
Plasmodium falciparum
mutant enzyme T618Q, at pH 7.4 and 25°C
-
0.00000155
4-[2-(fluorophenyl)-5-(1-methylpiperidine-4-yl)-1H pyrrol-3-yl] pyridine
Plasmodium falciparum
-
mutant enzyme T618M, in 50 mM HEPES, at pH 7.4, at 30°C
0.00000579
4-[2-(fluorophenyl)-5-(1-methylpiperidine-4-yl)-1H pyrrol-3-yl] pyridine
Plasmodium falciparum
-
wild type enzyme, in 50 mM HEPES, at pH 7.4, at 30°C
0.0178
4-[2-(fluorophenyl)-5-(1-methylpiperidine-4-yl)-1H pyrrol-3-yl] pyridine
Plasmodium falciparum
-
mutant enzyme T618Q, in 50 mM HEPES, at pH 7.4, at 30°C
0.00000045
4-[7-[(dimethylamino)methyl]-2-(4-fluorophenyl)-6-methylimidazo[1,2-a]pyridin-3-yl]-N-[4-(piperazin-1-yl)phenyl]pyrimidin-2-amine
Plasmodium falciparum
wild type enzyme, at pH 7.4 and 25°C
-
0.000231
4-[7-[(dimethylamino)methyl]-2-(4-fluorophenyl)-6-methylimidazo[1,2-a]pyridin-3-yl]-N-[4-(piperazin-1-yl)phenyl]pyrimidin-2-amine
Plasmodium falciparum
mutant enzyme T618Q, at pH 7.4 and 25°C
-
0.00000079
4-[7-[(dimethylamino)methyl]-2-(4-fluorophenyl)imidazo[1,2-a]pyridin-3-yl]-N-[4-(piperazin-1-yl)phenyl]pyrimidin-2-amine
Plasmodium falciparum
wild type enzyme, at pH 7.4 and 25°C
-
0.000842
4-[7-[(dimethylamino)methyl]-2-(4-fluorophenyl)imidazo[1,2-a]pyridin-3-yl]-N-[4-(piperazin-1-yl)phenyl]pyrimidin-2-amine
Plasmodium falciparum
mutant enzyme T618Q, at pH 7.4 and 25°C
-
0.0000031
4-[7-[(dimethylamino)methyl]-2-(4-fluorophenyl)imidazo[1,2-a]pyridine-3-yl]pyrimidin-2-amine
Plasmodium falciparum
wild type enzyme, at pH 7.4 and 25°C
0.0084
4-[7-[(dimethylamino)methyl]-2-(4-fluorophenyl)imidazo[1,2-a]pyridine-3-yl]pyrimidin-2-amine
Plasmodium falciparum
mutant enzyme T618Q, at pH 7.4 and 25°C
0.00000088
4-[7-[(dimethylamino)methyl]-2-[3-(methanesulfonyl)phenyl]imidazo[1,2-a]pyridin-3-yl]pyrimidin-2-amine
Plasmodium falciparum
wild type enzyme, at pH 7.4 and 25°C
-
0.1
4-[7-[(dimethylamino)methyl]-2-[3-(methanesulfonyl)phenyl]imidazo[1,2-a]pyridin-3-yl]pyrimidin-2-amine
Plasmodium falciparum
IC50 above 0.1 mM, mutant enzyme T618Q, at pH 7.4 and 25°C
-
0.0052
6'-methoxy-1,1':4',1''-terphenyl-2,2',5'-triol
Eimeria tenella
-
-
0.0104
6'-methoxy-1,1':4',1''-terphenyl-2,2',5'-triol
Toxoplasma gondii
-
-
0.0058
6'-methoxy-1,1':4',1''-terphenyl-2,2',5,5'-tetrol
Eimeria tenella
-
-
0.0095
6'-methoxy-1,1':4',1''-terphenyl-2,2',5,5'-tetrol
Toxoplasma gondii
-
-
0.00000434
N-(3-[3-(2-aminopyrimidin-4-yl)-7-[(dimethylamino)methyl]imidazo[1,2-a]pyridin-2-yl]phenyl)methanesulfonamide
Plasmodium falciparum
wild type enzyme, at pH 7.4 and 25°C
-
0.1
N-(3-[3-(2-aminopyrimidin-4-yl)-7-[(dimethylamino)methyl]imidazo[1,2-a]pyridin-2-yl]phenyl)methanesulfonamide
Plasmodium falciparum
IC50 above 0.1 mM, mutant enzyme T618Q, at pH 7.4 and 25°C
-
0.00000119
N-(5-[3-(2-aminopyrimidin-4-yl)-7-[(dimethylamino)methyl]-6-methylimidazo[1,2-a]pyridin-2-yl]-2-fluorophenyl)methanesulfonamide
Plasmodium falciparum
wild type enzyme, at pH 7.4 and 25°C
-
0.1
N-(5-[3-(2-aminopyrimidin-4-yl)-7-[(dimethylamino)methyl]-6-methylimidazo[1,2-a]pyridin-2-yl]-2-fluorophenyl)methanesulfonamide
Plasmodium falciparum
IC50 above 0.1 mM, mutant enzyme T618Q, at pH 7.4 and 25°C
-
0.00000079
N-(5-[3-(2-aminopyrimidin-4-yl)-7-[(dimethylamino)methyl]imidazo[1,2-a]pyridin-2-yl]-2-fluorophenyl)methanesulfonamide
Plasmodium falciparum
wild type enzyme, at pH 7.4 and 25°C
-
0.0737
N-(5-[3-(2-aminopyrimidin-4-yl)-7-[(dimethylamino)methyl]imidazo[1,2-a]pyridin-2-yl]-2-fluorophenyl)methanesulfonamide
Plasmodium falciparum
mutant enzyme T618Q, at pH 7.4 and 25°C
-
0.00000013
N-(cyclopropylmethyl)-4-[7-[(dimethylamino)methyl]-2-[3-(methanesulfonyl)phenyl]imidazo[1,2-a]pyridin-3-yl]pyrimidin-2-amine
Plasmodium falciparum
wild type enzyme, at pH 7.4 and 25°C
-
0.0525
N-(cyclopropylmethyl)-4-[7-[(dimethylamino)methyl]-2-[3-(methanesulfonyl)phenyl]imidazo[1,2-a]pyridin-3-yl]pyrimidin-2-amine
Plasmodium falciparum
mutant enzyme T618Q, at pH 7.4 and 25°C
-
0.00000016
N-[5-(3-[2-[(cyclopropylmethyl)amino]pyrimidin-4-yl]-7-[(dimethylamino)methyl]-6-methylimidazo[1,2-a]pyridin-2-yl)-2-fluorophenyl]methanesulfonamide
Plasmodium falciparum
wild type enzyme, at pH 7.4 and 25°C
-
0.02954
N-[5-(3-[2-[(cyclopropylmethyl)amino]pyrimidin-4-yl]-7-[(dimethylamino)methyl]-6-methylimidazo[1,2-a]pyridin-2-yl)-2-fluorophenyl]methanesulfonamide
Plasmodium falciparum
mutant enzyme T618Q, at pH 7.4 and 25°C
-
0.00000348
pyrrole 4-[2-(4-fluorophenyl)-5-(1-methylpiperidine-4-yl)-1H pyrrol-3-yl] pyridine
Plasmodium falciparum
-
IC50 for the recombinant FLAG-tagged enzyme 3.48 nM
0.00000835
pyrrole 4-[2-(4-fluorophenyl)-5-(1-methylpiperidine-4-yl)-1H pyrrol-3-yl] pyridine
Plasmodium falciparum
-
inhibits native and recombinant enzyme, shows antiparasitic activity being active against Plasmodium falsiparum blood cell stages cultured in vitro, IC50 for the native enzyme is 8.35 nM
0.0039
terferol
Eimeria tenella
-
-
0.0268
terferol
Toxoplasma gondii
-
-
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evolution
cGMP-dependent protein kinases belong to the group of serine/threonine kinases. The complete amino acid sequence of SmcGK1 indicates a greater similarity to type II cGKsof other organisms, but the sequence of SmcGK1 lacks a myristoylation motive typically found in mammalian membrane-bound cGKII, the homology to mammalian cGKII is mainly due to a high similarity of the kinase domains. SmcGK1 seems to occupy an intermediate position with respect to cGK classifications
evolution
-
cyclic GMP-dependent protein kinases constitute a small family of enzymes that are encoded by two genes
evolution
PKG maintains both its regulatory and catalytic elements on the same polypeptide chain.in contrast to PKA, EC 2.7.11.11
malfunction
-
accumulation of poly-ubiquitinated PKG-I induced by hypoxia is not affected by the endogenous activation of PKG-I by a cGMP analogue, or by the endogenous inhibition of PKG-I activity via a cell-permeable inhibitor
malfunction
-
acute inhibition of cGKI prevented stimulus-evoked enhancement of BKCa channel activity
malfunction
-
acute inhibition of cGKI prevents stimulus-evoked enhancement of BKCa channel activity
malfunction
enzyme inhibition leads to a multifaceted phenotype including slow motion, oocyte congestion, and reduced egg production
malfunction
-
PKG inhibition also potentiates the effect of SNAP on global cGMP levels and fully blocks the increase in cGMP-PDE5 activity
malfunction
-
blocking of the enzyme stops both replication and transmission of the Plasmodium falciparum
malfunction
-
enzyme inhibition decreases parasite egress from hepatocytes by inhibiting either the formation or release of merosomes
malfunction
-
enzyme inhibition modulates nicotine-induced currents mediated by nicotinic acetylcholine receptor2
malfunction
-
blockade of isoform PKG-I strongly slows cardiogenesis
malfunction
-
Drosophila embryos display targeting defects during axon development in the absence of the enzyme gene
malfunction
-
enzyme inhibition promotes uterine stromal cell proliferation
metabolism
-
cGMP-dependent protein kinase exerts a feedback control on cGMP concentration contributing to its intracellular compartmentation
metabolism
-
importance of the cGK-I/DAPK2 signaling pathway in regulating apoptosis, overview
metabolism
-
molecular mechanisms governing the transcriptional and posttranscriptional regulation of PKG-I expression in vascular smooth muscle cells, overview
metabolism
-
molecular mechanisms governing the transcriptional and posttranscriptional regulation of PKG-I expression in vascular smooth muscle cells, overview
metabolism
-
molecular mechanisms governing the transcriptional and posttranscriptional regulation of PKG-I expression in vascular smooth muscle cells, overview
metabolism
-
molecular mechanisms governing the transcriptional and posttranscriptional regulation of PKG-I expression in vascular smooth muscle cells, overview
metabolism
-
molecular mechanisms governing the transcriptional and posttranscriptional regulation of PKG-I expression in vascular smooth muscle cells, overview
metabolism
-
molecular mechanisms governing the transcriptional and posttranscriptional regulation of PKG-I expression in vascular smooth muscle cells, overview
metabolism
-
molecular mechanisms governing the transcriptional and posttranscriptional regulation of PKG-I expression in vascular smooth muscle cells, overview
metabolism
-
requirement for NO/cGMP/PKG signaling downstream of 17beta-estradiol for prevention of etoposide-induced death of MLO-Y4 osteocyte-like cells. BAD phosphorylation on Ser136 and Ser155 by Akt and PKG I, respectively, regulate BAD interaction with Bcl-2. NO activates soluble guanylate cyclase, generating cGMP, which in turn regulates cGMP-dependent protein kinases and phosphodiesterases. Estradiol-induced Akt and ERK activation in osteocytes is mediated by NO/cGMP/PKG II, and Akt is necessary for the anti-apoptotic effect of estradiol
physiological function
-
cGMP-dependent protein kinase is involved in the vasodilation of human saphenous veins
physiological function
-
cGMP-dependent protein kinase type I is an essential regulator of cellular function in blood vessels throughout the body
physiological function
-
cGMP-dependent protein kinase type I is an essential regulator of cellular function in blood vessels throughout the body
physiological function
-
cGMP-dependent protein kinase type I is an essential regulator of cellular function in blood vessels throughout the body
physiological function
-
cGMP production activates cGKII and induces the phosphorylation of GluA1, promoting its accumulation in the plasma membrane. Phosphorylation of GluA1 at Ser845 by type II cGMP-dependent protein kinase augments the surface expression of alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors at both synaptic and extrasynaptic sites. Activation of cGKII by 8-Br-cGMP enhances the surface expression of GluA1, whereas its inhibition or suppression effectively diminishes the expression of this protein at the cell surface, overview
physiological function
-
cGMP-dependent protein kinase exerts a feedback control on cGMP concentration contributing to its intracellular compartmentation, negative feedback of PKG on sGC-cGMP signaling attributable to PDE5 activation, kinetics and overview. PKG inhibition decreases and PKG activation increases cGMP-gated current. PKG activation in adult cardiomyocytes limits the accumulation of cGMP induced by NO donors via PDE5 stimulation but increases that induced by natriuretic peptides
physiological function
cGMP-dependent protein kinase serves as an integral component of second messenger signaling in a number of biological contexts including cell differentiation, memory, and vasodilation
physiological function
-
cGMP-dependent protein kinase-I (cGK-I) induces apoptosis in various cancer cell lines, and death-associated protein kinase 2, DAPK2, is one of the targets of cGK-I in apoptosis induction. Phosphorylation of DAPK2 at Ser299 by cGKI enhances DAPK2 kinase activity, but overexpression of a phospho-mimic DAPK2 mutant, DAPK2 S299D, as well as mutant S299D/S318E, strongly induce apoptosis in human breast cancer MCF-7 cells compared with wild-type DAPK2, while a S367D/S368D mutant does not
physiological function
-
PKG II is necessary for BAD Ser136 phosphorylation by Akt, allowing direct phosphorylation of Ser155 by PKG Ialpha. PKGIalpha and PKGII are independently required for estradiol- and cGMP-mediated protection against apoptosis, role of NO/cGMP signaling in 17beta-estradiol regulation of osteocyte survival
physiological function
-
PKG-I is a serine/threonine-specific protein kinase that is activated by the NO/sGC/cGMP system. PKG-I is involved in many cell functions, such as relaxation, platelet aggregation, remodelling, hypertrophy, apoptosis, differentiation, neuronal plasticity, and erectile dysfunction
physiological function
-
PKG-I is a serine/threonine-specific protein kinase that is activated by the NO/sGC/cGMP system. PKG-I is involved in many cell functions, such as relaxation, platelet aggregation, remodelling, hypertrophy, apoptosis, differentiation, neuronal plasticity, and erectile dysfunction
physiological function
-
PKG-I is a serine/threonine-specific protein kinase that is activated by the NO/sGC/cGMP system. PKG-I is involved in many cell functions, such as relaxation, platelet aggregation, remodelling, hypertrophy, apoptosis, differentiation, neuronal plasticity, and erectile dysfunction
physiological function
-
PKG-I is a serine/threonine-specific protein kinase that is activated by the NO/sGC/cGMP system. PKG-I is involved in many cell functions, such as relaxation, platelet aggregation, remodelling, hypertrophy, apoptosis, differentiation, neuronal plasticity, and erectile dysfunction
physiological function
-
PKG-I is a serine/threonine-specific protein kinase that is activated by the NO/sGC/cGMP system. PKG-I is involved in many cell functions, such as relaxation, platelet aggregation, remodelling, hypertrophy, apoptosis, differentiation, neuronal plasticity, and erectile dysfunction
physiological function
-
PKG-I is a serine/threonine-specific protein kinase that is activated by the NO/sGC/cGMP system. PKG-I is involved in many cell functions, such as relaxation, platelet aggregation, remodelling, hypertrophy, apoptosis, differentiation, neuronal plasticity, and erectile dysfunction
physiological function
-
PKG-I is a serine/threonine-specific protein kinase that is activated by the NO/sGC/cGMP system. PKG-I is involved in many cell functions, such as relaxation, platelet aggregation, remodelling, hypertrophy, apoptosis, differentiation, neuronal plasticity, and erectile dysfunction. PKG-I expression is controlled by RhoA and Rac1 activities. RhoA and Rac1 have opposing effects on PKG-I expression, with RhoA suppressing and Rac1 activating its promoter. RhoA regulation of the PKG-Ialpha promoter is mediated, at least in part, through binding of KLF4 to Sp1 consensus sites in the proximal promoter, which is located within the two Sp1 sites
physiological function
possible role of SmcGK1 during sexual development of schistosomes
physiological function
-
the activity of large conductance, Ca2+-activated K+ channels, i.e. BKCa channels, can be increased after modulation by type I cGMP-dependent protein kinase via nitric oxide/cGMP signaling
physiological function
-
the activity of large conductance, Ca2+-activated K+ channels, i.e. BKCa channels, can be increased after modulation by type I cGMP-dependent protein kinase via nitric oxide/cGMP signaling
physiological function
-
the enzyme is essential for the initiation of gametogenesis and for blood stage schizont rupture. Role for PfPKG during schizogony
physiological function
-
the enzyme plays an important role in the inhibition of cell proliferation and induction of apoptosis
physiological function
-
isoform PKG II activity attenuates basic fibroblast growth factorinduced proliferation and migration by inhibiting the MAPK/ERK signaling pathway in glioma cells, whereas isoform PKG I does not
physiological function
-
the cGMP/cGMP-dependent protein kinase signaling pathway is involved in this excitatory action of nitric oxide on Ca2+ channels
physiological function
-
the enzyme is required for sporozoite motility, invasion and merosome formation
physiological function
the enzyme present in cardiac smooth muscle cells or activated cardiac myofibroblasts is an important regulator of cardiac fibrosis
physiological function
-
the nuclear enzyme regulates the vascular smooth muscle cell phenotype
physiological function
-
type 2 cGMP-dependent protein kinase regulates homeostasis by blocking c-Jun N-terminal kinase in the colon epithelium
physiological function
-
isoform PKG2 is a key regulator of osteoblast proliferation and post-natal bone formation
physiological function
-
stimulation of enzyme activity preferentially reduces cell viability in the sphere phenotype of glioblastoma cells
physiological function
-
the enzyme has potential functions during decidualization
physiological function
-
the enzyme is required for CNS axon guidance. Enzyme overexpression leads to the cytoplasmic retention of transcription factor LolaT in S2 cells, suggesting a role for the enzyme in mediating the nucleocytoplasmic trafficking of Lola. The enzyme plays a role in regulating the establishment of neuronal connectivity by sequestering transcription factor Lola in the cytoplasm
physiological function
-
the presynaptic, but not postsynaptic or glial, enzyme gene is required for synaptic vesicle recycling. The enzyme gene FOR inhibits synaptic vesicle exocytosis during low-frequency stimulation by negatively regulating presynaptic Ca2+ levels and maintains neurotransmission during high-frequency stimulation by facilitating synaptic vesicle endocytosis. Additionally, glial FOR gene negatively regulated nerve terminal growth through TGF-beta signalling, and this developmental effect is independent of the effects of the enzyme gene on neurotransmission. Overall, the enzyme gene plays a critical role in coupling synaptic vesicle exocytosis and endocytosis, thereby balancing these two components to maintain sustained neurotransmission
physiological function
-
cGMP production activates cGKII and induces the phosphorylation of GluA1, promoting its accumulation in the plasma membrane. Phosphorylation of GluA1 at Ser845 by type II cGMP-dependent protein kinase augments the surface expression of alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors at both synaptic and extrasynaptic sites. Activation of cGKII by 8-Br-cGMP enhances the surface expression of GluA1, whereas its inhibition or suppression effectively diminishes the expression of this protein at the cell surface, overview
-
additional information
-
consensus motif for cGK is RR/KXS/T
additional information
docking studies with enzyme fragments PKG78-326, PKG78-341, and PKG78-355, a Cys117-Cys195 disulfide bond locks A and B helices in the A-domain and is involved in the metal-induced activation of PKG Ialpha, overview
additional information
-
the PKG-Ialpha isoform is more sensitive to ubiquitination compared with the PKG-Ibeta isoform
additional information
-
the PKG-Ialpha isoform is more sensitive to ubiquitination compared with the PKG-Ibeta isoform
additional information
-
the PKG-Ialpha isoform is more sensitive to ubiquitination compared with the PKG-Ibeta isoform
additional information
-
the PKG-Ialpha isoform is more sensitive to ubiquitination compared with the PKG-Ibeta isoform
additional information
-
the PKG-Ialpha isoform is more sensitive to ubiquitination compared with the PKG-Ibeta isoform
additional information
-
the PKG-Ialpha isoform is more sensitive to ubiquitination compared with the PKG-Ibeta isoform
additional information
-
the PKG-Ialpha isoform is more sensitive to ubiquitination compared with the PKG-Ibeta isoform
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PKG DELTA77
-
N-terminal deletion mutant, which lacks the dimerization domain
R77L
-
site-directed mutagenesis, the PKGIalpha mutation not only stabilizes the N-terminus but extends a stabilizing effect on the remaining domains of the enzyme as well
T770M
-
site-directed mutagenesis, mutant enzyme is not inhibited by pyrrole 4-[2-(4-fluorophenyl)-5-(1-methylpiperidine-4-yl)-1H-pyrrol-3-yl]pyridine
T770Q
-
site-directed mutagenesis, mutant enzyme is not inhibited by pyrrole 4-[2-(4-fluorophenyl)-5-(1-methylpiperidine-4-yl)-1H-pyrrol-3-yl]pyridine
C42L
the mutant shows similar temperature factors, which are consistently lower than those of wild type dimers
D412A/R415A
the mutant shows reduced activity compared to the wild type enzyme
I24A
-
site-directed mutagenesis, unaltered dimerization and molecular weight compared to the wild-type enzyme
L17A
-
site-directed mutagenesis, unaltered dimerization and molecular weight compared to the wild-type enzyme
L17A/I24A
-
site-directed mutagenesis, altered dimerization and molecular weight compared to the wild-type enzyme
L17A/I24A/L31A/I38A/L45A/I52A
-
site-directed mutagenesis, altered dimerization and molecular weight compared to the wild-type enzyme
L31A/I38A
-
site-directed mutagenesis, unaltered dimerization and molecular weight compared to the wild-type enzyme
L31A/I38A/L45A/I52A
-
site-directed mutagenesis, altered dimerization and molecular weight compared to the wild-type enzyme
L3A/L10A
-
site-directed mutagenesis, altered dimerization and molecular weight compared to the wild-type enzyme
L3A/L10A/L17A/I24A
-
site-directed mutagenesis, altered dimerization and molecular weight compared to the wild-type enzyme
L3A/L10A/L45A/I52A
-
site-directed mutagenesis, altered dimerization and molecular weight compared to the wild-type enzyme
R177A
-
the mutation in isoform PKG1alpha increases the basal activity of the enzyme
R177M
-
the mutation in isoform PKG1alpha increases the basal activity of the enzyme
R177Q
-
the mutation in isoform PKG1alpha increases PKG1alpha autophosphorylation in vitro and causes a high basal kinase activity (90-95%) in the absence of cGMP
R192Q
-
the mutation in isoform in PKG1beta increases PKG1beta autophosphorylation in vitro and causes a high basal kinase activity in the absence of cGMP
C43S
-
the mutant enzyme is less responsive to cGMP-induced activation with about 5fold reduced affinity for cGMP compared to the wild type enzyme
L58/72A
-
leucine zipper-deficient mutant
L72A
-
leucine zipper-deficient mutant
S79D
replacement of an autophosphorylated Ser79 of cGKIbeta with an aspartic acid results in a mutant kinase with constitutive kinase activity in vitro and in vivo. The cGKIbetaS79D mutant localized to the cytoplasm and is only a weak activator of CRE-dependent gene transcription
D533A
-
the mutant shows strongly reduced activity compared to the wild type enzyme
Q532A
-
the mutant shows strongly reduced activity compared to the wild type enzyme
R484A
-
the mutant shows strongly reduced activity compared to the wild type enzyme
R484A/Q532A/D533A
-
the mutant shows strongly reduced activity compared to the wild type enzyme
T618M
-
the amino acid substitution does not confer insensitivity to 4-[2-(fluorophenyl)-5-(1-methylpiperidine-4-yl)-1H pyrrol-3-yl] pyridine
K482A
-
site-directed mutagenesis, transfection of the catalytically inactive PKGII mutant inhibits aldosterone production in zona glomerulosa cells
R242Q
-
the partially activated mutant enzyme expressed in primary osteoblasts of transgenic mice shows a 2-3fold increase in basal and total isoform PKG2 activity; they proliferate faster and are resistant to apoptosis compared to cells from wild type mice
S110A/S114A/S445A
-
site-directed mutagenesis, the mutant shows 60% reduced autophosphorylation activity compared to the wild-type GKII
T761M
-
site-directed mutagenesis, mutant enzyme is not inhibited by pyrrole 4-[2-(4-fluorophenyl)-5-(1-methylpiperidine-4-yl)-1H-pyrrol-3-yl]pyridine
T761Q
-
site-directed mutagenesis, mutant enzyme is not inhibited by pyrrole 4-[2-(4-fluorophenyl)-5-(1-methylpiperidine-4-yl)-1H-pyrrol-3-yl]pyridine
T618Q
-
mutant is over 3000fold less sensitive to 4-[2-(fluorophenyl)-5-(1-methylpiperidine-4-yl)-1H pyrrol-3-yl] pyridine and shows 10-20fold lower sensitivity to 4-[7-[(dimethylamino)methyl]-2-(4-fluorophenyl)imidazo[1,2-a]pyridine-3-yl]pyrimidin-2-amine than the wild type enzyme
T618Q
the mutant exhibits a reduced sensitivity to many inhibitors of between 500 and more than 100000fold as compared to the wild type enzyme
E589A
inactive
additional information
-
construction of a DELTA1-77 truncation mutant
additional information
-
overexpression in Xenopus laevis of either guanylate cyclase or PKG in embryos increases acetylcholine receptor aggregate area by 60170%, whereas expression of a dominant negative form of guanylate cyclase inhibits endogenous aggregation by 50%, overview
additional information
construction of enzyme fragments PKG78-326, PKG78-341, and PKG78-355. Mutational disruption of the Knob-Nest interface in full-length PKG Ia decreases the activation constant and suggests a tethering mechanism for the catalytic domain
additional information
-
construction of the gain-of-function mutant egl-4 of PKG, mutation causes increased normal gene activity although it is associated with a reduced EGL-4 protein level, multiple phenotypes of egl-4 dominant mutants, detailed analysis, overview, isolation of egl-4 loss-of-function mutations in cis to ad450sd and of extragenic suppressors of ad450sd, overview
additional information
-
construction of transgenic flies by targeted expression of DG2P1 and DG2P2, and DG1 in malpigian tubule using the UAS/GAL4 system, differential localization of all 3 enzyme forms in transgenic flies, phenotypes, overview
additional information
-
constructed PKG-knockout mutant parasite strains are refractory to to inhibitor pyrrole 4-[2-(4-fluorophenyl)-5-(1-methylpiperidine-4-yl)-1H-pyrrol-3-yl]pyridine with reduced sensitivity, complementation by expression of Toxoplasma gondii PKG
additional information
-
construction of a PKG Ibeta leucine zipper mutant, and of the deletion mutant DELTA1-52 lacking the N-terminal part, mutants show slightly altered properties, overview
additional information
-
construction of a PKG-Ibeta deletion mutant DELTA1-52
additional information
-
expression of constitutively active enzyme prevents glucose stimulation of thrombospondin 1 expression and TGF-beta activity
additional information
-
the enzyme is inactivated by expression of a dominant negative mutant PKG construct
additional information
-
enzyme inhibition by a dominant negative PKG construct G1alphaR-GFP, enzyme inhibition blocks apoptosis in suspended CCD841 cells
additional information
-
expression of wild-type and mutant human serotonin transporters in HeLa cells and effects on activation through phosphorylation by PKG and cell metabolism, overview
additional information
-
overexpression of active PKGIalpha, but not of the inactive mutant K390A, increases of Akt and inhibits necrosis and apoptosis in cardiomyocytes, overview
additional information
-
construction of cGKI knockout mice
additional information
-
construction of PKGI knockout mutant mice, phenotype analysis, platelet secretion, platelet aggregation, and Ca2+ mobilization are affected
additional information
-
construction of tissue-specific cGK-knockout mice causing several dysfunction phenotypes, overview
additional information
-
PKG-I knockout mutant mice show no induction of p38 by thrombin
additional information
-
PKGII-deficient mice are defective in renal functiona regulation, and in resetting the circadian clock because light induction of mPer2 gene in the hypothalamus is strongly reduced in the early peroid of the night, whereas mPer1 gene induction is elevated
additional information
-
primary myoblast of enzyme-deficient mice mutants show excessive cell fusion
additional information
-
during ischemia and reperfusion in vivo, mice with a cardiac myocyte-restricted deletion of PKG I display a more pronounced interaction of TAB1 with p38MAPK and a stronger phosphorylation of p38 MAPK in the myocardial area at risk during reperfusion and more apoptotic cardiac myocytes in the infarct border zone as compared to wild-type littermates
additional information
-
during ischemia and reperfusion in vivo, mice with a cardiac myocyte-restricted deletion of PKG I display a more pronounced interaction of TAB1 with p38MAPK and a stronger phosphorylation of p38 MAPK in the myocardial area at risk during reperfusion and more apoptotic cardiac myocytes in the infarct border zone as compared to wild-type littermates
-
additional information
injection of PKG-Ialpha-specific antisense or overexpression constructs into two-cell stage embryos causes severe abnormalities in the developing embryos, phenotypes, overview
additional information
injection of PKG-Ialpha-specific antisense or overexpression constructs into two-cell stage embryos causes severe abnormalities in the developing embryos, phenotypes, overview
additional information
-
injection of PKG-Ialpha-specific antisense or overexpression constructs into two-cell stage embryos causes severe abnormalities in the developing embryos, phenotypes, overview
additional information
injection of PKG-Ibeta-specific antisense or overexpression constructs into two-cell stage embryos causes severe abnormalities in the developing embryos, phenotypes, overview
additional information
injection of PKG-Ibeta-specific antisense or overexpression constructs into two-cell stage embryos causes severe abnormalities in the developing embryos, phenotypes, overview
additional information
-
injection of PKG-Ibeta-specific antisense or overexpression constructs into two-cell stage embryos causes severe abnormalities in the developing embryos, phenotypes, overview
additional information
-
constructing PKG I-DELTAN1-92, a PKG I mutant lacking the N-terminal 92 amino acids
additional information
-
siRNA-mediated down-regulation of RhoA derepresses PKG I expression
additional information
-
constructed PKG-knockout mutant parasite strains are refractory to to inhibitor pyrrole 4-[2-(4-fluorophenyl)-5-(1-methylpiperidine-4-yl)-1H-pyrrol-3-yl]pyridine with reduced sensitivity, complementation by expression of Eimeria tenella PKG
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