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2.7.3.2: creatine kinase

This is an abbreviated version!
For detailed information about creatine kinase, go to the full flat file.

Word Map on EC 2.7.3.2

Reaction

ATP
+
Creatine
=
ADP
 +
phosphocreatine

Synonyms

adenosine triphosphate-creatine transphosphorylase, adenosine-5'-triphosphate: creatine phosphotransferase, ATP-creatine transphosphorylase, ATP: creatine N-phosphotransferase, ATP:creatine phosphotransferase, B-type creatine kinase, BB-CK, BB-type creatine kinase, BCK, brain creatine kinase, brain type creatine kinase, brain-type CK, brain-type creatine kinase, CK, CK MM, CK-B, CK-BB, CK-MB, CK-MM, ckb, CKM, CKMB, CKMBI, CKMiMi, creatine kinase, creatine kinase B, creatine kinase M-type, creatine kinase MB, creatine kinase muscle type, creatine kinase-MB, creatine N-phosphotransferase, creatine phosphokinase, creatine phosphotransferase, creatinine kinase, creatinine kinase MB, hBBCK, hMMCK, kinase, creatine (phosphorylating), M-CK, M1-CK, MB-CK, MCK, Mi-CK, MiMi-CK, mit-CK, mitochondrial creatine kinase, MM-CK, MM-type creatine kinase, More, MtCK, muscle creatine kinase, muscle type creatine kinase, muscle-type creatine kinase, phosphocreatine kinase, plasma creatine kinase, PSCKM, recombinant human brain-type creatine kinase, rHBCK, RM-CK, s-type CK, sarcomeric CK, sMiCK, sMtCK, u-type CK, ubiquitous CK, ubiquitous MtCK, uMiCK, uMtCK, zMMCK

ECTree

     2 Transferases
         2.7 Transferring phosphorus-containing groups
             2.7.3 Phosphotransferases with a nitrogenous group as acceptor
                2.7.3.2 creatine kinase

Inhibitors

Inhibitors on EC 2.7.3.2 - creatine kinase

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INHIBITOR
ORGANISM
UNIPROT
COMMENTARY hide
LITERATURE
IMAGE
(2Z)-3-butyl-1-phenyl-2-(phenyltellanyl)oct-2-en-1-one
-
organotellurium inhibits creatine kinase activity by two different mechanisms: competition with ADP and oxidation of critical sulfhydryl groups for the functioning of the enzyme
1-anilinonaphthalene-8-sulfonate
unfolding agent
2,3-butadiene
-
complete inhibition, MgATP2- or MgADP- protect the enzyme from inactivation
4,4'-dithiodipyridine
-
-
4-hydroxy-2-nonenal
-
dose-dependent inhibition of creatine kinase, inhibition correlates with 4-hydroxy-2-nonenal adduct formation on specific amino acid residues including the active site residues H66, H191, C283, and H296
4-hydroxy-3-nitrophenylglyoxal
-
complete inactivation, modification of 2 arginine residues per enzyme subunit, inhibition kinetics at pH 8.7, MgATP2- or MgADP- protect the enzyme from inactivation
4-hydroxymercuribenzoic acid
5,5'-dithiobis(2-nitrobenzoate)
5-(4-([(benzoylphenyl)amino]carbonyl)phenyl)-2-furoic acid
-
35% inhibition, docking energy -49.5 kcal/mol
5-(4-([(biphenyl-4-ylmethyl)amino]carbony)phenyl)-2-furoic acid
-
63% inhibition, docking energy -51.8 kcal/mol
5-(4-benzoylbiphenyl-4-yl)-2-furoic acid
-
63% inhibition, docking energy -46.3 kcal/mol
5-(4-[(benzylamino)carbonyl]phenyl)-2-furoic acid
-
20% inhibition, docking energy -47.4 kcal/mol
5-(4-[[(benzoylphenyl)amino]carbonyl]phenyl)-2-furoic acid
-
-
5-(4-[[(biphenyl-4-ylmethyl)amino]carbony]phenyl)-2-furoic acid
-
-
5-[4-[(benzylamino)carbonyl]phenyl]-2-furoic acid
-
-
acetaminophen
-
inhibits creatine kinase in cerebellum and hippocampus, the administration of N-acetylcysteine plus deferoxamine reverses the inhibition of creatine kinase activity
Acrylamide
alpha-P-borano substituted ADP Sp isomer
-
strong competitive inhibitor
Bis-Tris
-
-
bovine serum albumin
-
no influence on enzyme activity
-
Ca2+
-
-
carbon tetrachloride
-
inhibits creatine kinase activity in cerebellum, the administration of N-acetylcysteine plus deferoxamine reverses the inhibition of creatine kinase activity
catechin
-
-
Cd2+
-
Cd2+ conspicuously inactivates the activity of the muscle-type enzyme in a first-order kinetic process and exhibits non-competitive inhibition with creatine and ATP. Cd2+ induces tertiary structure changes in enzyme PSCKM with exposure of hydrophobic surfaces. The addition of osmolytes, such as glycine and proline, partially reactivates the enzyme. Molecular dynamics and docking simulations between PSCKM and Cd2+ show that Cd2+ blocks the entrance of ATP to the active site of the enzyme, computational modeling, overview
Chromium ADP
-
competitive to MgADP-
Chromium ATP
-
competitive to MgATP2-
clozapine
-
inhibition of enzyme in cerebellum and prefrontal cortex after chronic administration
copper metabolism gene MURR1 domain 6
-
0.006 mg is capable of inhibiting the activities of both the MM- and BB-type creatine kinases
-
Creatinine phosphate
Cu2+
-
-
cystine
cystine dimethylester
-
-
ethylmalonic acid
-
accumulation in patients affected by short-chain acyl-CoA dehydrogenase deficiency and other diseases. Ethylmalonic acid inhibits the activity of respiratory chain complexes and also inhibits creatine kinase at concentrations o 1 mM and 5 mM
Fe3+
-
-
formate
guanidine hydrochloride
in the absence of added guanidine hydrochloride, MM-CK activity slightly decreases with NaCl concentration up to 4 M, but a dramatic decline is observed above that value, with full inactivation at 4.5 M. When guanidine is added, curves with similar shapes are obtained but NaCl concentrations needed to inactivate the enzyme are shifted towards lower values
Guanidinium chloride
inhibitory, in presence of NaCl, increased inhibitory activity. Inactivation by NaCl is due to dissociation of dimeric creatine kinase into its constitutive subunits, and upon monomerization, the protein becomes more susceptible to guanidinium denaturing effect
guanidinium hydrochloride
Guanidinoacetate
-
vitamins E and C prevent the effects of intrastriatal administration of guanidinoacetate on the inhibition of creatine kinase
H2O2
irreversible inhibition. H2O2 interacts with the ADP binding region of the active site of the enzyme. Enzymatic activity is rapidly abolished with less than 1 mM H2O2. Any residual activity is completely lost at an H2O2 concentration of 2-10 mM; irreversible inhibition. The enzyme activity rapidly abolishes with less than 1 mM H2O2. Any residual activity is completely lost at an H2O2 concentration of 2-10 mM. Adding reducing agents such as 2 mM dithiothreitol, 4 mM N-acetyl-l-cysteine, or 4 mM reduced L-glutathione before H2O2 treatment prevents against inactivation caused by 0.5 mM H2O2. However, if antioxidants are added 1 h after addition of 0.5 mM H2O2, no recovery is observed compared with the H2O2-treated group
imidazole
-
-
iodoacetamide
iodoacetic acid
Iodoethane
-
-
jujubogenin
-
L-arginine
-
treatment with single injection or for one week with daily injection of saline or L-Arg plus Nomega-nitro-L-arginine methyl ester or alpha-tocopherol plus ascorbic acid. Total and cytosolic creatine kinase activities are significantly inhibitied by L-arginine adminstration, mitochondrial enzyme activity is not affected. simultaneous injection of Nomega-nitro-L-arginine methyl ester and alpha-tocopherol plus ascorbic acid prevent inhibition
L-isoleucine
-
branched chain alpha-amino acids bind at the active site, competitive inhibition mechanism against substrates phosphocreatine and ADP, inhibition kinetics
L-leucine
-
branched chain alpha-amino acids bind at the active site, competitive inhibition mechanism against substrates phosphocreatine and ADP, inhibition kinetics
L-lysine
-
total and cytosolic creatine kinase activities are significantly inhibited by L-lysine, in contrast to the mitochondrial isoform which is not affected, the inhibitory effect of L-lysine on total creatine kinase activity is totally prevented by reduced glutathione
L-valine
-
branched chain alpha-amino acids bind at the active site, competitive inhibition mechanism against substrates phosphocreatine and ADP, inhibition kinetics
Lactic acid
-
induces dissociation of enzyme dimer and unfolding of the enzyme at 0.8 mM, but no aggregation at 25°C or 40°C even at high protein concentrations, inactivation kinetics
LiCl
-
inactivation due to subunit dissociation, mechanism
luteolin
-
-
MOPS buffer
-
i.e. 3-(N-morpholino)propane sulfonate
morphine
0.00001-0.1 mM morphine significantly reduces recombinant enzymatic activity (27% inhibition at 0.001 mM, 80% inhibition at more than 0.05 mM); 27% inhibition at 0.001 m, 80% inhibition at more than 0.05 mM
N-ethylmaleimide
-
-
nitrate
nitrite
NO2-
-
-
p-hydroxymercuribenzoate
-
-
Pb2+
-
lead inhibits in vitro the cytosolic and mitochondrial creatine kinase activity at 0.2 mM and that this inhibition is prevented by addition cysteamine to the assay at 0.1 mM and 0.5 mM final concentration
Phenylglyoxal
-
complete inactivation, reacts on arginine residues
phosphate
-
competitive against ATP and phosphocreatine, noncompetitive against ADP and creatine
Pipes buffer
-
i.e. 1,4-piperazine diethanesulfonic acid
quercetin
-
mechanism, role of radicals
SO32-
-
-
SO42-
-
-
sodium barbital
-
slow inactivation of enzyme that can be reversed by dilution. Sodium barbital may compete mainly with creatine, but also with ATP, for inhibition
sulfate
-
competitive against ATP and phosphocreatine, noncompetitive against ADP and creatine
taxifolin
-
-
thiosulfate
-
0.5 mM thiosulfate administration decreases the enzyme activity 30 min after administration. Thiosulfate also decreases the activity of the enzyme in vitro in striatum of rats, which is prevented by the thiol reducing agents dithiothreitol, the antioxidants glutathione, melatonin, trolox, and lipoic acid; thiosulfate (1 M) inhibits creatine kinase activity in rat striatum via thiol group oxidation is prevented by the thiol reducing agents dithiothreitol GSH, melatonin, trolox and lipoic acid
trans-[RuCl2(3-pyridinecarboxylic acid)4]
-
administration at 180.7 micromol/kg, inhibition of creatine kinase activity in hippocampus, striatum, cerebral cortex, heart and skeletal muscle. No effect on enzyme in vitro
transition state analogue complex
-
Tris
-
-
additional information
-