2.7.3.2	(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	3049	
2.7.3.2	1-anilinonaphthalene-8-sulfonate	unfolding agent	127453	
2.7.3.2	2,3-butadiene	complete inhibition, MgATP2- or MgADP- protect the enzyme from inactivation	127455	
2.7.3.2	4,4'-dithiodipyridine	-	6845	
2.7.3.2	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	1426	
2.7.3.2	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	127454	
2.7.3.2	4-hydroxymercuribenzoic acid	-	8382	
2.7.3.2	4-hydroxymercuribenzoic acid	complete inhibition at 0.01 mM	8382	
2.7.3.2	5,5'-dithiobis(2-nitrobenzoate)	-	303	
2.7.3.2	5,5'-dithiobis(2-nitrobenzoate)	less than 5% residual activity at 0.1 mM	303	
2.7.3.2	5-(4-([(benzoylphenyl)amino]carbonyl)phenyl)-2-furoic acid	35% inhibition, docking energy -49.5 kcal/mol	61961	
2.7.3.2	5-(4-([(biphenyl-4-ylmethyl)amino]carbony)phenyl)-2-furoic acid	63% inhibition, docking energy -51.8 kcal/mol	135152	
2.7.3.2	5-(4-benzoylbiphenyl-4-yl)-2-furoic acid	63% inhibition, docking energy -46.3 kcal/mol	62641	
2.7.3.2	5-(4-[(benzylamino)carbonyl]phenyl)-2-furoic acid	20% inhibition, docking energy -47.4 kcal/mol	135153	
2.7.3.2	5-(4-[[(benzoylphenyl)amino]carbonyl]phenyl)-2-furoic acid	-	69111	
2.7.3.2	5-(4-[[(biphenyl-4-ylmethyl)amino]carbony]phenyl)-2-furoic acid	-	143975	
2.7.3.2	5-[4-[(benzylamino)carbonyl]phenyl]-2-furoic acid	-	143974	
2.7.3.2	acetaminophen	inhibits creatine kinase in cerebellum and hippocampus, the administration of N-acetylcysteine plus deferoxamine reverses the inhibition of creatine kinase activity	2541	
2.7.3.2	Acrylamide	significantly inactivate screatine kinase and glutathione S-transferase and deplete glutathione. When the dietary constituents, tea polyphenols, resveratrol, and diallyl trisulfide are cotreated with acrylamide, all of them can effectively recover the activities of creatine kinase	1914	
2.7.3.2	Acrylamide	CK-BB is kinetically reversibly inactivated by acrylamide accompanied by the disruption of the hydrophobic surface, complete inhibition at 800 mM	1914	
2.7.3.2	alpha-P-borano substituted ADP Sp isomer	strong competitive inhibitor	69110	
2.7.3.2	ATP	-	4	
2.7.3.2	Bis-Tris	-	43877	
2.7.3.2	bovine serum albumin	no influence on enzyme activity	274	
2.7.3.2	Br-	-	332	
2.7.3.2	Ca2+	-	15	
2.7.3.2	carbon tetrachloride	inhibits creatine kinase activity in cerebellum, the administration of N-acetylcysteine plus deferoxamine reverses the inhibition of creatine kinase activity	8476	
2.7.3.2	catechin	-	1437	
2.7.3.2	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	52	
2.7.3.2	Chromium ADP	competitive to MgADP-	96282	
2.7.3.2	Chromium ATP	competitive to MgATP2-	97823	
2.7.3.2	Cl-	-	141	
2.7.3.2	Cl-	inactivation at -17°C	141	
2.7.3.2	clozapine	inhibition of enzyme in cerebellum and prefrontal cortex after chronic administration	4685	
2.7.3.2	Co2+	-	23	
2.7.3.2	copper metabolism gene MURR1 domain 6	0.006 mg is capable of inhibiting the activities of both the MM- and BB-type creatine kinases	155586	
2.7.3.2	Creatine	-	433	
2.7.3.2	Creatinine phosphate	competitive to phosphocreatine	43943	
2.7.3.2	Creatinine phosphate	competitive to MgATP2-	43943	
2.7.3.2	Cu2+	-	19	
2.7.3.2	cystine	cystine inhibited the enzyme activity in a dose- and time-dependent manner and cysteamine prevents and reverses the inhibition caused by cystine, suggesting that cystine inhibits creatine kinase activity by oxidation of the sulfhydryl groups of the enzyme; dose- and time-dependent inhibition, cysteamine prevents and reverses this inhibition	1967	
2.7.3.2	cystine	inhibits creatine kinase activity possibly by oxidation of the sulfhydryl groups of the enzyme. Considering that creatine kinase like other thiol-containing enzymes, is crucial for energy homeostasis and antioxidant defenses, the enzymes inhibition caused by cystine released from lysosomes could be one of the mechanisms of tissue damage in patients with cystinosis	1967	
2.7.3.2	cystine dimethylester	-	143973	
2.7.3.2	DTNB	-	554	
2.7.3.2	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	135613	
2.7.3.2	F-	-	174	
2.7.3.2	Fe3+	-	70	
2.7.3.2	formate	mimics the phosphoryl group in the transition state	120	
2.7.3.2	glycocyamine	-	10661	
2.7.3.2	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	1048	
2.7.3.2	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	2558	
2.7.3.2	guanidinium hydrochloride	inactivation mechanism of wild-type and mutant enzymes, overview	3124	
2.7.3.2	guanidinium hydrochloride	first dissociation of subunits, then unfolding into random coil	3124	
2.7.3.2	guanidinium hydrochloride	0.1-3.0 M, under both conditions, the tag-free enzyme shows the lowest degree of aggregation, followed by His-tagged CK, and Fc-III-tagged CK has the highest degree of aggregation	3124	
2.7.3.2	Guanidinoacetate	vitamins E and C prevent the effects of intrastriatal administration of guanidinoacetate on the inhibition of creatine kinase	1788	
2.7.3.2	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	22	
2.7.3.2	I-	-	507	
2.7.3.2	imidazole	-	470	
2.7.3.2	iodoacetamide	-	67	
2.7.3.2	iodoacetamide	protection by MgATP2-, MgADP-, urea	67	
2.7.3.2	iodoacetamide	substrates can protect against alkylation	67	
2.7.3.2	iodoacetamide	70.9% inhibition of the atypical ubiquitous mitochondrial enzyme, 74.6% inhibition of the typical ubiquitous mitochondrial enzyme	67	
2.7.3.2	iodoacetic acid	-	213	
2.7.3.2	Iodoethane	-	8117	
2.7.3.2	iodomethane	-	4534	
2.7.3.2	jujubogenin	16.9% inhibition at 0.005 mM	256836	
2.7.3.2	jujubogenin	-	256836	
2.7.3.2	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	123	
2.7.3.2	L-isoleucine	branched chain alpha-amino acids bind at the active site, competitive inhibition mechanism against substrates phosphocreatine and ADP, inhibition kinetics	311	
2.7.3.2	L-leucine	branched chain alpha-amino acids bind at the active site, competitive inhibition mechanism against substrates phosphocreatine and ADP, inhibition kinetics	127	
2.7.3.2	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	134	
2.7.3.2	L-valine	branched chain alpha-amino acids bind at the active site, competitive inhibition mechanism against substrates phosphocreatine and ADP, inhibition kinetics	246	
2.7.3.2	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	7226	
2.7.3.2	LiCl	inactivation due to subunit dissociation, mechanism	815	
2.7.3.2	luteolin	-	436	
2.7.3.2	MOPS buffer	i.e. 3-(N-morpholino)propane sulfonate	44432	
2.7.3.2	additional information	haloperidol, no effect on enzyme. Aripiprazole, no effect on enzyme in hippocampus, cerebellum and prefrontal cortex	2	
2.7.3.2	additional information	no effect: trans-[RuCl2(4-pyridinecarboxylic acid)4]	2	
2.7.3.2	additional information	cysteamine, glutathione, and sodium acetate does not affect cytosolic and mitochondrial creatine kinase activity	2	
2.7.3.2	additional information	transition state analogue complex substrates inhibit the dimeric but not the octameric enzyme; transition state analogue complex substrates inhibit the dimeric but not the octameric enzyme	2	
2.7.3.2	additional information	lansoprazole at 0.003 mg/ml does not alter DNA integrity of human spermatozoa or activity of seminal creatine kinase after 1 h incubation period; there is no significant change in the activity of seminal creatine kinase by the effect of lansoprazole (0.003 mg/ml, 1 h incubation)	2	
2.7.3.2	additional information	brain creatine kinase activity is lower on days 14 and 21 post-feeding in animals that receive aflatoxin B1-contaminated diet compared to the control group. The inhibition of brain enzyme activity appears to be mediated by the oxidation of lipids, proteins, and thiol group, as well as by a reduction in the antioxidant capacity	2	
2.7.3.2	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	1050	
2.7.3.2	N-ethylmaleimide	-	49	
2.7.3.2	NaCl	inactivation due to subunit dissociation, mechanism	42	
2.7.3.2	NaCl	enzyme activity slightly decreases with NaCl concentration up to 4 M, and a dramatic decline is observed above that value, with full inactivation at 4.5 M. In presence of guanidinium chloride, inactivation occurs much earlier. 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; 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	42	
2.7.3.2	nitrate	mimics the phosphoryl group in the transition state	308	
2.7.3.2	nitrite	mimics the phosphoryl group in the transition state	168	
2.7.3.2	NO2-	-	852	
2.7.3.2	NO3-	inactivation at -17°C	673	
2.7.3.2	NO3-	-	673	
2.7.3.2	p-hydroxymercuribenzoate	-	98	
2.7.3.2	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	139	
2.7.3.2	Phenylglyoxal	complete inactivation, reacts on arginine residues	301	
2.7.3.2	phosphate	competitive against ATP and phosphocreatine, noncompetitive against ADP and creatine	16	
2.7.3.2	Pipes buffer	i.e. 1,4-piperazine diethanesulfonic acid	94780	
2.7.3.2	quercetin	mechanism, role of radicals	137	
2.7.3.2	SDS	dissociation of subunits, no unfolding	124	
2.7.3.2	SDS	strongly inhibits the CK-BB activity in a noncompetitive manner, although almost all the activity is eliminated by SDS CK-BB is never completely inactivated (4% to 5% activity is still sustained), regardless of increased incubation time or SDS concentration	124	
2.7.3.2	SO32-	-	902	
2.7.3.2	SO42-	-	245	
2.7.3.2	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	31919	
2.7.3.2	sulfate	competitive against ATP and phosphocreatine, noncompetitive against ADP and creatine	160	
2.7.3.2	taxifolin	-	3233	
2.7.3.2	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	475	
2.7.3.2	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	36430	
2.7.3.2	transition state analogue complex	consists of creatine, MgADP, and planar ions such as nitrate, nitrite, and formate, binding structure	57778	
2.7.3.2	transition state analogue complex	creatine, MgADP-, and planar ions such as nitrate, nitrite, and formate	57778	
2.7.3.2	Tris	-	317	
2.7.3.2	Zn2+	-	14	
2.7.3.2	Zn2+	Zn2+ may induce CK-BB inactivation and misfolding, when the Zn2+ concentration is 0.4 mM, CK-BB activity is completely abolished	14