2.7.4.21: inositol-hexakisphosphate 5-kinase
This is an abbreviated version!
For detailed information about inositol-hexakisphosphate 5-kinase, go to the full flat file.
Word Map on EC 2.7.4.21
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2.7.4.21
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pyrophosphate
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polyphosphate
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pp-insps
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tetrakisphosphate
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ppip5ks
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bis-diphosphoinositol
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pyrophosphorylation
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5-insp7
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5-diphosphoinositol
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medicine
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ptdins3,4,5p3
- 2.7.4.21
- pyrophosphate
- polyphosphate
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pp-insps
- tetrakisphosphate
- ppip5ks
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bis-diphosphoinositol
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pyrophosphorylation
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5-insp7
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5-diphosphoinositol
- medicine
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ptdins3,4,5p3
Reaction
Synonyms
AtIPK2alpha, AtIpk2beta, ATP:1D-myo-inositol-hexakisphosphate phosphotransferase, AtVip1, AtVip2, diphosphoinositol pentakisphosphate kinase 2, diphosphoinositol pentakisphosphate synthetase, EC 2.7.1.152, EhIP6KA, IHPK2, inositol hexakisphosphate 5-kinase, inositol hexakisphosphate kinase, inositol hexakisphosphate kinase 1, inositol hexakisphosphate kinase 2, inositol hexakisphosphate kinase 3, inositol hexakisphosphate kinase type 2, inositol hexakisphosphate kinase-1, inositol hexakisphosphate kinase-2, inositol hexakisphosphate kinase-3, inositol polyphosphate kinase, inositol-hexakisphosphate kinase, InsP6 kinase, InsP6-kinase, InsP6K1, InsP6K2, InsP6K3, IP6 kinase, IP6 kinase 1, IP6K, IP6K1, IP6K2, IP6K3, Ipk2, IPMK, Kcs1, kinase (phosphorylating), inositol hexakisphosphate, More, Pi uptake stimulator, PiUS, PPIP5K1, PPIP5K2, RID-2
ECTree
2.7.4.21 inositol-hexakisphosphate 5-kinaseAdvanced search results
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results (Engineering
Engineering on EC 2.7.4.21 - inositol-hexakisphosphate 5-kinase
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PROTEIN VARIANTS 
ORGANISM
UNIPROT
COMMENTARY 
LITERATURE
D292A
K248A
the mutant shows a reduction in 1D-myo-inositol hexakisphosphate-stimulated ATPase activity of isofom PPIP5K2. The mutant shows a significant reduction in the rate of 1D-myo-inositol phosphate-independent ATPase activity of isofom PPIP5K2
R213A
the mutant shows a reduction in 1D-myo-inositol hexakisphosphate-stimulated ATPase activity of isofom PPIP5K2
R332A
2.4-4fold larger net formation of 1D-myo-inositol 5-diphosphate 1,2,3,4,6-pentakisphosphate, but mutation nearly completely impaires its hydrolysis
R388A
2.4-4fold larger net formation of 1D-myo-inositol 5-diphosphate 1,2,3,4,6-pentakisphosphate, but mutation nearly completely impaires its hydrolysis
R837H
variant R837H segregates with DFNB100-associated hearing loss. Mutation reduces the phosphatase activity of PPIP5K2 and elevates its kinase activity
K217A
a kinase-dead mutant IP6K3, the catalytically inactive IP6K3 K217A mutant binds spectrin/adducin similarly to the wild-type enzyme
R133A
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mutation of IP6K2 in its putative HSP90-binding motif, mutation of Arg133 abolishes IP6K2-HSP90 binding
R136A
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mutation of IP6K2 in its putative HSP90-binding motif, mutation of Arg136 abolishes IP6K2-HSP90 binding
S118A/S121A
site-directed mutagenesis, no phosphorylation of IP6K1 mutant S118A-S121A in HEK293 cells. The mutant does not efficiently bind Myc-PLIN1 in HEK293 cells
S347A/S359A
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site-directed mutagenesis, the mutant displays 3.5fold greater TAK1 activation following TNF-alpha, the mutant demonstrates a 6-10fold increase in NF-kappaB DNA binding following TNF-alpha compared with wild type IHPK2-expressing cells in which NF-kappa B DNA binding is inhibited
S85A
site-directed mutagenesis, the mutation does not influence its binding to Myc-PLIN1 in HEK293 cells
W131A
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mutation of IP6K2 in its putative HSP90-binding motif, mutation of Trp131 modestly diminishes IP6K2-HSP90 binding, the catalytically impaired IP6K2-W131A does not induce cell death
additional information
additional information
construction of a atipk2alpha/atipk2beta double mutant with male gametophyte and embryogenesis defects, the mutant cannot be rescued by either catalytically inactive or substrate specificity-altered variants of AtIPK2beta. The single knock-out mutant of atipk2alpha is indistinguishable from the wild-type. Transmission analysis of atipk2alpha and atipk2beta mutant alleles and Segregation analysis of atipk2alpha and atipk2beta mutants, overview. Complementation analysis of the atipk2alpha/atipk2beta double mutant, development-defective phenotype
additional information
construction of a atipk2alpha/atipk2beta double mutant with male gametophyte and embryogenesis defects, the mutant cannot be rescued by either catalytically inactive or substrate specificity-altered variants of AtIPK2beta. The single knock-out mutant of atipk2alpha is indistinguishable from the wild-type. Transmission analysis of atipk2alpha and atipk2beta mutant alleles and Segregation analysis of atipk2alpha and atipk2beta mutants, overview. Complementation analysis of the atipk2alpha/atipk2beta double mutant, development-defective phenotype
additional information
construction of a atipk2alpha/atipk2beta double mutant with male gametophyte and embryogenesis defects, the mutant cannot be rescued by either catalytically inactive or substrate specificity-altered variants of AtIPK2beta. The single knock-out mutant of atipk2beta is indistinguishable from the wild-type. Transmission analysis of atipk2alpha and atipk2beta mutant alleles and Segregation analysis of atipk2alpha and atipk2beta mutants, overview. Complementation analysis of the atipk2alpha/atipk2beta double mutant, development-defective phenotype
additional information
construction of a atipk2alpha/atipk2beta double mutant with male gametophyte and embryogenesis defects, the mutant cannot be rescued by either catalytically inactive or substrate specificity-altered variants of AtIPK2beta. The single knock-out mutant of atipk2beta is indistinguishable from the wild-type. Transmission analysis of atipk2alpha and atipk2beta mutant alleles and Segregation analysis of atipk2alpha and atipk2beta mutants, overview. Complementation analysis of the atipk2alpha/atipk2beta double mutant, development-defective phenotype
additional information
construction of an Entamoeba histolytica hybrid IP6K/IP3K chimeric hybrid through molecular modeling and mutagenesis
additional information
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construction of an Entamoeba histolytica hybrid IP6K/IP3K chimeric hybrid through molecular modeling and mutagenesis
additional information
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NLS (nuclear localization sequence) mutant of IHPK2 (4 point mutations in the NLS) remains in the cytoplasm, even after interferon-beta treatment
additional information
construction of an N-terminally truncated mutant PPIP5K2KD comprising residues 41-366
additional information
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construction of an inactive enzyme mutant, overexpression of wild-type IHPK2 sensitizes ovarian carcinoma cell lines to the growth-suppressive and apoptotic effects of interferon beta, IFN-alpha2, and gamma-irradiation. Expression of a kinase-dead mutant abrogates 50% of the apoptosis induced by IFN-beta
additional information
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depletion of IP6K2 in HEK-293 cells by RNAi leads to 40-50% reduced cell death, overview. Deletion mapping of IP6K2 to identify HSP90-binding motif, overview. The yeast Saccharomyces cerevisiae possesses constitutive and inducible homologues of HSP90, designated HSC82 and HSP82, respectively. In HSC82 KO yeast, IP6K activity is 2.5fold higher than murine wild-type, in yeast HSP82 null mutant, IP6K catalytic activity is increased but to a lesser extent. Overexpression of HSP90 markedly reduces IP6K catalytic activity in HEK-293 cells
additional information
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gene deletion of IP6K1 in mice leads to markedly diminished production of inositol diphosphates. Male mutant mice are sterile with defects in spermiogenesis. Mutant mice are smaller than wild-type despite normal food intake. The mutants display markedly lower circulating insulin, phenotype, overview
additional information
construction of IP6K1 knockout MEF cells. Deletion of the Q2 domain results in decreased nuclear localization in more than 60% of cells
additional information
generation of enzyme-deficient Ip6k1-/- mice, phenotype, overview
additional information
IP6K3 knockdown HEK293 cells are generated by lentiviral transduction. Diminished cerebellar synapses in IP6K3 mutants
additional information
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generation of enzyme-deficient Ip6k1-/- mice, phenotype, overview
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