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(DL)-propargylglycine
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chronical treatment of rats with CGL inhibitor (DL)-propargylglycine or cystathionine beta-synthase inhibitor aminooxyacetic acid or a combination of both. Only the rats with combination therapy show a decrease in urinary sulfate excretion rate, which is associated with an increase in mean arterial pressure. Urine flow and sodium excretion are also increased in combination group as consequent to the increase in mean arterial pressure. Glomerular filtration rate does not alter due to these treatments, renal blood flow is lowered only in the combination group compared to the control group
1,10-phenanthroline
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2 mM, 20% inhibition
1-nitroso-2-naphthol-3,6-disulfonic acid
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2 mM, 55% inhibition
2-(4-methoxyanilino)-2-oxoethyl-(2E)-2-[(3-fluoropyridin-2-yl)methylidene]hydrazine-1-carbodithioate
compound shows at least 400fold selectivity for CSEgamma over inhibition of cystathionine beta-synthase
2-(prop-2-yn-1-ylamino)acetic acid
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-
3-methyl-2-benzothiazolinone
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31% residual activity at 5 mM
3-Methyl-2-benzothiazolinone hydrazone
4-chloromercuribenzoate
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-
5,5'-dithiobis(2-nitrobenzoate)
6-diazo-5-oxonorleucine
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-
8-Hydroxyquinoline-5-sulfonic acid
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2 mM, 13% inhibition
acetoacetate
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treatment with 0.025-0.035 mM H2O2, 4-8 mM acetoacetate and high D-glucose of 25 mM causes a significant decrease in enzyme protein expression, enzyme activity, and H2S levels, and an increase in intracellular reactive oxygen species production compared with those in normal controls
AgNO3
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alpha,beta-elimination L-homoserine
alpha-amino-gamma-aminooxybutanoate
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-
aminoethoxyvinylglycine
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-
beta,beta,beta-trifluoroalanine
beta-cyano-L-Ala
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alpha,beta-elimination L-homoserine
beta-trifluoromethyl-D,L-Ala
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i.e. 2-amino-4,4,4-trifluorobutanoate
CH3-Hg-S-Cys
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the cysteine S-conjugate of Hg2+ is a potent irreversible enzyme inhibitor
Cys-S-Hg-S-Cys
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the cysteine S-conjugate of Hg2+ is a potent irreversible enzyme inhibitor
D-glucose
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treatment with 0.025-0.035 mM H2O2, 4-8 mM acetoacetate and high D-glucose of 25 mM causes a significant decrease in enzyme protein expression, enzyme activity, and H2S levels, and an increase in intracellular reactive oxygen species production compared with those in normal controls
DL-Penicillamine
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3% residual activity at 5 mM
EDTA
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2 mM, 13% inhibition
H2O2
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treatment with 0.025-0.035 mM H2O2, 4-8 mM acetoacetate and high D-glucose of 25 mM causes a significant decrease in enzyme protein expression, enzyme activity, and H2S levels, and an increase in intracellular reactive oxygen species production compared with those in normal controls
HgCl2
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a potent irreversible enzyme inhibitor, but HgCl2 is also a strong inactivator of cystathionine gamma-lyase
iodoacetamide
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22% residual activity at 2.5 mM
Isonicotinic acid hydrazide
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-
L-aminoethoxyvinylglycine
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-
L-beta-oxalyl amino-L-alanine
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inhibition only after long exposure
N-prop-2-yn-1-ylglycine
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-
NEM
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0.05 mM, inhibition is partly relieved by 0.2 mM 2,3-dimercaptopropanol
O2
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homogenized gills produces H2S enzymatically, and H2S production is inhibited by O2, whereas mitchondrial H2S consumption is O2 dependent
Sodium cyanide
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alpha,beta-elimination, 1 mM, 82% inhibition
streptozotocin
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livers from streptozotocin-treated type I diabetic rats have lower levels of enzyme protein expression, enzyme activity, reduced tissue H2S formation, and increased reactive oxygen species production compared with those of controls
3-Methyl-2-benzothiazolinone hydrazone
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-
3-Methyl-2-benzothiazolinone hydrazone
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-
5,5'-dithiobis(2-nitrobenzoate)
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8 of the 12 -SH groups in native enzyme react reversibly. Cystathionine at high concentrations, partially relieves the inhibition
5,5'-dithiobis(2-nitrobenzoate)
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aminooxyacetic acid
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aminooxyacetic acid
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chronical treatment of rats with CGL inhibitor (DL)-propargylglycine or cystathionine beta-synthase inhibitor aminooxyacetic acid or a combination of both. Only the rats with combination therapy show a decrease in urinary sulfate excretion rate, which is associated with an increase in mean arterial pressure. Urine flow and sodium excretion are also increased in combination group as consequent to the increase in mean arterial pressure. Glomerular filtration rate does not alter due to these treatments, renal blood flow is lowered only in the combination group compared to the control group
beta,beta,beta-trifluoroalanine
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the epsilon-NH2 group of the active-site Lys forms a Schiff base with pyridoxal 5'phosphate is capable of interacting with the beta carbon of the suicide inactivator beta,beta,beta-trifluoroalanine
beta,beta,beta-trifluoroalanine
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-
beta,beta,beta-trifluoroalanine
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irreversible
Beta-cyano-L-alanine
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-
Beta-cyano-L-alanine
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pretreating adiopose tissues with the CSE inhibitor beta-cyano-L-alanine (BCA) (2 mmol/l) for 20 min significantly decreased the endogenous H2S production by 89%, as compared with controls
Beta-cyano-L-alanine
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10 mM inhibits testosterone induced H2S biosynthesis
Beta-cyanoalanine
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-
Beta-cyanoalanine
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reversible inhibitor of CSE
cycloserine
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DL-cycloserine
cycloserine
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partially competitive
cycloserine
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D-cycloserine
Cys
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-
Cys
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the regulatory site of the enzyme is specific for L-Cys
Cys
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above 10 mM, inhibits replacement reaction with L-homoserine and L-Cys
DL-propargylglycine
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-
DL-propargylglycine
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irreversible inhibitor of CSE
DL-propargylglycine
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irreversible inhibitor
DL-propargylglycine
an irreversible enzyme inhibitor, molecular mechanism of DL-propargylglycine action in vivo
DL-propargylglycine
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2% residual activity at 5 mM
DL-propargylglycine
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elevates blood pressure
DL-propargylglycine
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irreversible inhibitor of CSE
DL-propargylglycine
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pretreating adiopose tissues with the CSE inhibitor DL-propargylglycine (PPG) (10 mmol/l) for 20 min significantly decreased the endogenous H2S production by 85%, as compared with controls
DL-propargylglycine
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irreversible inhibitor of CSE
DL-propargylglycine
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irreversible inhibitor of CSE
DL-propargylglycine
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selective inhibitor of cystathionine gamma-lyase
Hg2+
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strong
Hg2+
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HgCl2, alpha,beta-elimination L-homoserine
hydroxylamine
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-
hydroxylamine
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alpha,beta-elimination of L-homoserine
L-cysteine
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0.4 mM, 6% residual activity
L-cysteine
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substrate inhibition mainly due to removal of cofactor
L-cysteine
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inhibits alpha,gamma elimination activity
N-ethylmaleimide
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81% residual activity at 5 mM
NaCl
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5% w/v
NaCl
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59% residual activity at 5 mM
PCMB
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0.05 mM, inhibition is partly relieved by 0.2 mM 2,3-dimercaptopropanol
PCMB
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alpha,beta-elimination L-homoserine
Penicillamine
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D-penicillamine; L-penicillamine
Penicillamine
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D-penicillamine; L-penicillamine
Penicillamine
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alpha,beta-elimination of L-homoserine; D-penicillamine; L-penicillamine
phenylhydrazine
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2.8% residual activity at 5 mM
phenylhydrazine
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alpha,beta-elimination L-homoserine as substrate
propargylglycine
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-
propargylglycine
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10 mM inhibits testosterone induced H2S biosynthesis
propargylglycine
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alpha,beta-elimination L-homoserine
Semicarbazide
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-
Semicarbazide
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11% residual activity at 5 mM
Semicarbazide
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alpha,beta-elimination L-homoserine as substrate
trifluoro-Ala
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-
trifluoro-Ala
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trifluoro-D,L-Ala
Zn2+
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0.1 mM, weak
Zn2+
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ZnCl2, alpha,beta-elimination L-homoserine
additional information
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no or poor inhibition by methylselenocysteine, D-cycloserine, pargyline, and parsalmide
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additional information
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no inhibition by 4-hydroxybutyrate
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additional information
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not inhibitory: EDTA
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additional information
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the reaction of cystathionase with cystathionine and homoserine decreases rapidly with time. The reaction becomes inhibited, probably by the formation of a stable enzyme-bound intermediate. The inhibition can be partially relieved by pyridoxal 5'-phosphate, NaCl, alpha-keto acids, and other compounds. These agents prevent the inhibition by providing an environment that helps to decrease the nucleophilicity of the sulfhydryl
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additional information
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inhibitory effect of the chelating agents and related compounds is at least partly and in some instances completely eliminated in the presence of an increased concentration of pyridoxal 5'-phosphate
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additional information
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administration of CSE inhibitors enhances the glucose uptake of adipocytes
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additional information
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dexamethasone reduces the expression of cystathionine gamma lyase. Also reduces LPS-induced upregulation of CSE in fetal liver cells. 6-amino-4-(4-phenoxyphenylethylamino) quinazoline (QNZ) 10 nM, a selective inhibitor of transcription via the NF-kappaB pathway, abolishs lipopolysaccharide-induced upregulation of CSE expression
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additional information
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extent to which inactivation occurs with the various mercury-containing compounds in descending order: Cys-S-Hg-S-Cys, HgCl2, CH3Hg-S-Cys
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additional information
cystathionine gamma-lyase encoded by CYS3 is repressed by addition of cysteine to the growth medium
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additional information
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cystathionine gamma-lyase encoded by CYS3 is repressed by addition of cysteine to the growth medium
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