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(2R)-1-(2-formyl-3,6-dihydroxy-5-methoxycyclohexa-1,4-dien-1-yl)tridecan-2-yl acetate
-
-
(2R)-1-(2-hydroxy-5-methoxy-3,6-dioxocyclohexa-1,4-dien-1-yl)pentadecan-2-yl acetate
-
-
(2R)-1-(2-hydroxy-5-methoxy-3,6-dioxocyclohexa-1,4-dien-1-yl)tridecan-2-yl acetate
-
-
(2R)-1-(3,6-dihydroxy-5-methoxycyclohexa-1,4-dien-1-yl)tridecan-2-yl acetate
-
-
(2R)-1-(5-methoxy-3,6-dioxocyclohexa-1,4-dien-1-yl)pentadecan-2-yl acetate
-
-
(2R)-1-(5-methoxy-3,6-dioxocyclohexa-1,4-dien-1-yl)tridecan-2-yl acetate
-
-
(2R)-1-[3-(acetyloxy)-6-hydroxy-5-methoxycyclohexa-1,4-dien-1-yl]pentadecan-2-yl acetate
-
-
(2R)-1-[3-(acetyloxy)-6-hydroxy-5-methoxycyclohexa-1,4-dien-1-yl]tridecan-2-yl acetate
-
-
(2S)-1-(5-methoxycyclohexa-1,4-dien-1-yl)heptan-2-ol
-
-
(2S)-2-amino-6-imino-5-oxohexanoic acid
-
1,2-naphthoquinone 4-sulfonate
-
-
1-amino-8-naphthol-2,4-disulfonic acid
-
weak
2,2-dimethyl-5-[4-(methylsulfanyl)phenyl]-2,3,5,6-tetrahydrobenzo[a]phenanthridin-4(1H)-one
-
97% inhibition at 0.05 mM
2,2-dimethyl-5-[4-(naphthalen-1-yl)phenyl]-2,3,5,6-tetrahydrobenzo[a]phenanthridin-4(1H)-one
-
97% inhibition at 0.05 mM
2,2-dimethyl-5-[4-(propan-2-yl)phenyl]-2,3,5,6-tetrahydrobenzo[a]phenanthridin-4(1H)-one
-
91% inhibition at 0.05 mM
2,4-dinitro-1-naphthol-7-sulfonic acid
-
i.e. flavianic acid
2-bromo-4-(2,2-dimethyl-4-oxo-1,2,3,4,5,6-hexahydrobenzo[a]phenanthridin-5-yl)-6-methoxyphenyl acetate
-
84% inhibition at 0.05 mM
2-hydroxy-5-methoxy-3-tridecylcyclohexa-2,5-diene-1,4-dione
-
-
2-methoxy-6-pentadecylcyclohexa-2,5-diene-1,4-dione
-
-
2-methoxy-6-tridecylcyclohexa-2,5-diene-1,4-dione
-
-
2-methyl-5-[(7Z)-pentadec-7-en-1-yl]cyclohexa-1,4-diene-1,3-diol
-
-
2-methyl-5-[(7Z)-tridec-7-en-1-yl]cyclohexa-1,4-diene-1,3-diol
-
-
2-phenyl isoindolin-1-one
-
-
2-phenylbenzo[d] isoxazol-3(2H)-one
-
-
2-phenylbenzo[d]isothiazol-3(2H)-one
-
-
3-[(2S)-2-hydroxypentadecyl]-5-methoxycyclohexa-2,5-dien-1-ol
-
-
4-hydroxy-2-methoxy-6-(2-oxopentadecyl)cyclohexa-2,5-dien-1-yl acetate
-
-
5,5'-(sulfanediyldiethane-2,1-diyl)bis(1,3,4-thiadiazol-2-amine)
-
5-(3-bromo-4,5-dimethoxyphenyl)-2,2-dimethyl-2,3,5,6-tetrahydrobenzo[a]phenanthridin-4(1H)-one
-
complete inhibition at 0.05 mM
5-(3-bromo-4-(dimethylamino)phenyl)-2,2-dimethyl-2,3,5,6-tetrahydrobenzo[a]phenanthridin-4(1H)-one
-
-
5-(3-chloro-4,5-dimethoxyphenyl)-2,2-dimethyl-2,3,5,6-tetrahydrobenzo[a]phenanthridin-4(1H)-one
-
88% inhibition at 0.05 mM
5-(4-tert-butylphenyl)-2,2-dimethyl-2,3,5,6-tetrahydrobenzo[a]phenanthridin-4(1H)-one
-
99% inhibition at 0.05 mM
5-[(6Z)-13-(3,5-dihydroxy-4-methylcyclohexa-1,4-dien-1-yl)tridec-6-en-1-yl]-2-methylbenzene-1,3-diol
-
-
5-[(6Z)-13-(3,5-dihydroxy-4-methylcyclohexa-1,4-dien-1-yl)tridec-6-en-1-yl]benzene-1,3-diol
-
-
5-[(6Z)-13-(3-hydroxy-5-methoxycyclohexa-1,4-dien-1-yl)tridec-6-en-1-yl]benzene-1,3-diol
-
-
5-[(7Z)-13-(3-hydroxy-5-methoxyphenyl)tridec-7-en-1-yl]-2-methylcyclohexa-1,4-diene-1,3-diol
-
-
5-[(7Z)-15-(3-hydroxy-5-methoxyphenyl)pentadec-7-en-1-yl]-2-methylcyclohexa-1,4-diene-1,3-diol
-
-
5-[(7Z)-pentadec-7-en-1-yl]cyclohexa-1,4-diene-1,3-diol
-
-
5-[(7Z)-tridec-7-en-1-yl]cyclohexa-1,4-diene-1,3-diol
-
-
5-[(8Z)-15-(3,5-dihydroxy-4-methylcyclohexa-1,4-dien-1-yl)pentadec-8-en-1-yl]-2-methylbenzene-1,3-diol
-
-
5-[(8Z)-15-(3,5-dihydroxy-4-methylcyclohexa-1,4-dien-1-yl)pentadec-8-en-1-yl]benzene-1,3-diol
-
-
5-[(8Z)-15-(3-hydroxy-5-methoxycyclohexa-1,4-dien-1-yl)pentadec-8-en-1-yl]benzene-1,3-diol
-
-
5-[14-(3-hydroxy-5-methoxycyclohexa-1,4-dien-1-yl)tetradecyl]benzene-1,3-diol
-
-
5-[3-bromo-4-(dimethylamino)phenyl]-2,2-dimethyl-2,3,5,6-tetrahydrobenzo[a]phenanthridin-4(1H)-one
5-[4-(diethylamino)phenyl]-2,2-dimethyl-2,3,5,6-tetrahydrobenzo[a]phenanthridin-4(1H)-one
-
96% inhibition at 0.05 mM
5-[4-(dimethylamino)phenyl]-2,2-dimethyl-2,3,5,6-tetrahydrobenzo[a]phenanthridin-4(1H)-one
-
59% inhibition at 0.05 mM
5-[5-[(phenylacetyl)amino]-1,3,4-thiadiazol-2-yl]-N-[2-(4-phenylpiperidin-1-yl)ethyl]pentanamide
-
5-[5-[(phenylacetyl)amino]-1,3,4-thiadiazol-2-yl]-N-[2-(piperidin-1-yl)ethyl]pentanamide
-
5-[5-[(phenylacetyl)amino]-1,3,4-thiadiazol-2-yl]-N-[2-(pyrrolidin-1-yl)ethyl]pentanamide
-
5-[5-[(phenylacetyl)amino]-1,3,4-thiadiazol-2-yl]-N-[4-(trifluoromethyl)benzyl]pentanamide
-
6-diazo-5-oxo-L-norleucine
6-diazo-5-oxo-Lnorleucine
-
time-dependent inhibition
8-[3-bromo-4-(diethylamino)phenyl]-11,11-dimethyl-8,10,11,12-tetrahydrobenzo[a][4,7]phenanthrolin-9(7H)-one
-
96% inhibition at 0.05 mM
8-[3-bromo-4-(dimethylamino)phenyl]-11,11-dimethyl-8,10,11,12-tetrahydrobenzo[a][4,7]phenanthrolin-9(7H)-one
-
91% inhibition at 0.05 mM
Al3+
-
46% residual activity at 1 mM
anthraquinone-1,8-disulfonate
-
-
apomorphine
-
competitive inhibition, i.e. 5,6,6a,7-tetrahydro-6-methyl-4H-dibenzo[de,g]quinoline-10,11-diol
arsenate
-
0.5 M, 74% inhibition
azaserine
about 19% inhibition at about 1 mM
BaCl2
-
inhibition to a variable extent
bicarbonate
-
0.5 M, complete inhibition
bis-2-(5-phenylacetamido-1,2,4-thiadiazol-2-yl) ethyl sulfide
-
i.e. BPTES, binds to an allosteric pocket at the dimer interface of kidney-type glutaminase, triggering a dramatic conformational change of the key loop (Glu312-Pro329) near the catalytic site and rendering it inactive, allosteric inhibition. Binding of BPTES stabilizes the inactive tetramers of the catalytic domain of kidney-type glutaminase. The binding mode of BPTES on the hydrophobic pocket determines its specificity to the kidney-type glutaminase isoform KGA
bis-2-(5-phenylacetamido-1,2,4-thiadiazol-2-yl)ethyl sulfide
bis-2-(5-phenylacetimido-1,2,4,thiadiazol-2-yl)ethyl sulfide
inhibits specifically GLS1 and its splice variant GAC, two inhibitor molecules bind at an interface region of the GAC tetramer in a manner that appears to lock the GAC tetramer into a nonproductive conformation, binding structure and mechanism of glutaminase inhibition, overview; inhibits specifically GLS1 splice variant GAC, two inhibitor molecules bind at an interface region of the GAC tetramer in a manner that appears to lock the GAC tetramer into a nonproductive conformation, binding structure and mechanism of glutaminase inhibition, overview
bis-2-(5-phenylacetimido-1,2,4-thiadiazol-2-yl) ethyl sulfide
-
glutaminase-1-selective inhibitor
bis-2-(5-phenylacetimido-1,2,4-thiadiazol-2-yl)ethyl sulfide
-
uncompetitive inhibition
CaCl2
-
inhibition to a variable extent
CB-839
i.e. N-[5-[4-[6-[[2-[3-(trifluoromethoxy)phenyl]acetyl]amino]-3-pyridazinyl]butyl]-1,3,4-thiadiazol-2-yl]-2-pyridineacetamide, is the best inhibitor as designated by the binding free energy changes
Cd2+
-
complete inhibition at 50 mM
chelerythrine
-
competitive inhibition, i.e. 1,2-dimethoxy-N-methyl[1,3]benzodioxolo[5,6-c]phenanthridinium
citrate
-
enzyme from mesenteric lymph nodes
Cl-
-
0.5 M, complete inhibition
CN-
-
0.5 M, complete inhibition
CoCl2
-
14% inhibition at 1 mM
compound 968
-
i.e. 5-(3-bromo-4-(dimethylamino)phenyl)-2,2-dimethyl-2,3,5,6-tetrahydrobenzo[a]phenanthridin-4(1H)-one, combined with erlotinib down-regulates the glutamine and glycolysis metabolism in erlotinib-resistant non-small cell lung cancer cells
CuCl2
-
20% inhibition at 1 mM, 17% at 0.1 mM
CuSO4
-
inhibition to a variable extent
D-glucose
-
negative influence in media with glucose as carbon source
dimethyl 2-[1-(4-tert-butylbenzoyl)-2,2,7-trimethyl-3-methylidene-2,3-dihydroquinolin-4(1H)-ylidene]-1,3-dithiole-4,5-dicarboxylate
-
97% inhibition at 0.05 mM
diphenylarsinic acid
-
the protein level of GAC significantly decrease in an concentration manner. The PAG activities are also decreased in parallel with the decrease in GAC
diphosphate
-
0.1 M, 98% inhibition
ebselen
-
mixed non-competitive inhibition, i.e. 2-phenyl-1,2-benzisoselenazol-3[2H]-one
glufosinate ammonium
about 23% inhibition at about 1 mM
L-Glutamic acid
Triticale sp.
-
5 mM, about a 40% inhibition
L-methionine sulfoximine
about 21% inhibition at about 1 mM
metformin
-
68% inhibition at 100 mM
methylene blue
-
0.005%, irreversible inactivation
MgCl2
-
20% inhibition at 1 mM, 12% at 0.1 mM
MnCl2
-
22% inhibition at 1 mM, 13% at 0.1 mM
N'-[(E)-[3-bromo-4-(dimethylamino)phenyl]methylidene]-2-(9-oxoacridin-10(9H)-yl)acetohydrazide
-
93% inhibition at 0.05 mM
N,N'-[sulfanediylbis(ethane-2,1-diyl-1,3,4-thiadiazole-5,2-diyl)]bis(2-phenylacetamide)
-
N-(2-aminoethyl)-5-[5-[(phenylacetyl)amino]-1,3,4-thiadiazol-2-yl]pentanamide
-
N-(5-[2-[2-(5-amino-[1,3,4]thiadiazol-2-yl)-ethylsulfanyl]-ethyl]-[1,3,4]thiadiazol-2-yl)-2-phenyl-acetamide
-
N-benzyl-5-[5-[(phenylacetyl)amino]-1,3,4-thiadiazol-2-yl]pentanamide
-
N-bromosuccinimide
-
5 mM, 19% of initial activity
N-methyl-5-[5-[(phenylacetyl)amino]-1,3,4-thiadiazol-2-yl]-N-[2-(pyrrolidin-1-yl)ethyl]pentanamide
-
N-tert-butyl-5-[5-[(phenylacetyl)amino]-1,3,4-thiadiazol-2-yl]pentanamide
-
N-tert-butyl-N-methyl-5-[5-[(phenylacetyl)amino]-1,3,4-thiadiazol-2-yl]pentanamide
-
N-[2-(1-methylpyrrolidin-2-yl)ethyl]-5-[5-[(phenylacetyl)amino]-1,3,4-thiadiazol-2-yl]pentanamide
-
N-[2-(4-hydroxypiperidin-1-yl)ethyl]-5-[5-[(phenylacetyl)amino]-1,3,4-thiadiazol-2-yl]pentanamide
-
N-[2-(diethylamino)ethyl]-5-[5-[(phenylacetyl)amino]-1,3,4-thiadiazol-2-yl]pentanamide
-
N-[4-(dimethylamino)benzyl]-5-[5-[(phenylacetyl)amino]-1,3,4-thiadiazol-2-yl]pentanamide
-
N-[4-[4-(5-amino-1,3,4-thiadiazol-2-yl)butyl]-1,3-thiazol-2-yl]-2-phenylacetamide
-
N-[5-(2-[[2-(5-amino-1,3,4-thiadiazol-2-yl)ethyl]sulfinyl]ethyl)-1,3,4-thiadiazol-2-yl]-2-phenylacetamide
-
N-[5-[2-(5-amino-1,3,4-thiadiazol-2-yl)ethyl]-1,3,4-thiadiazol-2-yl]-2-phenylacetamide
-
N-[5-[4-(5-amino-1,3,4-thiadiazol-2-yl)butyl]-1,3,4-thiadiazol-2-yl]-2-(4-fluorophenyl)acetamide
-
N-[5-[4-(5-amino-1,3,4-thiadiazol-2-yl)butyl]-1,3,4-thiadiazol-2-yl]-2-(4-methylphenyl)acetamide
-
N-[5-[4-(5-amino-1,3,4-thiadiazol-2-yl)butyl]-1,3,4-thiadiazol-2-yl]-2-cyclohexylacetamide
-
N-[5-[4-(5-amino-1,3,4-thiadiazol-2-yl)butyl]-1,3,4-thiadiazol-2-yl]-2-phenylacetamide
-
N-[5-[4-(5-amino-1,3,4-thiadiazol-2-yl)butyl]-1,3,4-thiadiazol-2-yl]-2-phenylpropanamide
-
N-[5-[4-(5-amino-1,3,4-thiadiazol-2-yl)butyl]-1,3,4-thiadiazol-2-yl]-3-phenylpropanamide
-
N-[5-[4-(5-amino-1,3,4-thiadiazol-2-yl)butyl]-1,3,4-thiadiazol-2-yl]benzamide
-
N-[5-[4-(5-amino-1,3,4-thiadiazol-2-yl)butyl]-1,3-thiazol-2-yl]-2-phenylacetamide
-
Na2SO4
-
glutaminase I and II
NaCIO4
-
0.3 M, 25% inhibition
NaF
-
inhibition to a variable extent
NaH2PO4
-
0.3 M, complete inhibition
NaN3
-
complete inhibition at 1 mM
NaNO3
-
0.3 M, 15% inhibition
Ngamma,Ngamma-diethyl-L-glutamine
-
-
Ngamma,Ngamma-dimethyl-L-glutamine
-
-
Ngamma-ethyl-L-glutamine
-
-
Ngamma-methyl-L-glutamine
-
-
nitrite
-
0.5 M, complete inhibition
O-(diazoacetyl)-L-serine
-
-
p-chloromercuribenzoate
-
p-chloromercuribenzoic acid
-
complete inhibition at 10 mM
Pb2+
-
69.27% residual activity at 100 mM
phenylarsonic acid
-
causes a decrease in GAC levels
phenylmethylarsinic acid
-
causes a decrease in GAC levels
protein BNIP-H
i.e. Caytaxin or brain-specific BNIP-2-homology protein, encoded by gene ATCAY, important in neuromal function, inhibits the enzyme and alters its steady-state kinetics, relocalises glutaminase to neurite terminals and reduces glutamate levels in vivo, effects on glutamate levels in overexpressing cell lines, e.g. murine Neuro2A cells or rat PC-12 cells, or in female rat brain, detailed overview
-
R(-)-propylnorapomorphine
-
-
Rose bengal
-
0.01%, irreversible inactivation
succinate
-
enzyme from mesenteric lymph nodes
TLCK
-
5 mM, 12% of initial activity
Tris
-
0.5 M, complete inhibition
ZnCl2
-
7% inhibition at 1 mM
2-oxoglutarate
-
enzyme from mesenteric lymph nodes
2-oxoglutarate
-
competitive inhibition
5-[3-bromo-4-(dimethylamino)phenyl]-2,2-dimethyl-2,3,5,6-tetrahydrobenzo[a]phenanthridin-4(1H)-one
-
5-[3-bromo-4-(dimethylamino)phenyl]-2,2-dimethyl-2,3,5,6-tetrahydrobenzo[a]phenanthridin-4(1H)-one
-
95% inhibition at 0.05 mM
6-diazo-5-oxo-L-norleucine
-
-
6-diazo-5-oxo-L-norleucine
-
6-diazo-5-oxo-L-norleucine
-
-
6-diazo-5-oxo-L-norleucine
-
6-diazo-5-oxo-L-norleucine
-
blockade of PAG, avoids the toxic effects of Gln accumulation in the brain
6-diazo-5-oxo-L-norleucine
-
-
6-diazo-5-oxo-L-norleucine
active site inhibitor, about 53% inhibition at about 1 mM
6-diazo-5-oxo-L-norleucine
-
10 mM, strongly inhibited, 80% inhibition, especially more strongly with a progress of purification steps
6-diazo-5-oxo-L-norleucine
-
-
6-diazo-5-oxo-L-norleucine
-
-
6-diazo-5-oxo-L-norleucine
-
-
6-diazo-5-oxo-L-norleucine
-
-
bis-2-(5-phenylacetamido-1,2,4-thiadiazol-2-yl)ethyl sulfide
-
bis-2-(5-phenylacetamido-1,2,4-thiadiazol-2-yl)ethyl sulfide
-
a potent inhibitor of kidney-type glutaminase, but not of the liver-type glutaminase, glutamate dehydrogenase or gamma-glutamyl transpeptidase. The potent inhibitor causes the formation of a stable, but inactive, tetramer
Ca2+
-
10 mM, 80% of initial activity
Ca2+
-
72.59% residual activity at 100 mM
Ca2+
-
0.5-1.0 mM, NEM-sensitive enzyme
Co2+
-
90% residual activity at 1 mM
Co2+
-
70.53% residual activity at 100 mM
Co2+
-
5 mM, 81% of initial activity
Cu2+
-
10 mM, 44% of initial activity
Cu2+
-
complete inhibition at 50 mM
Cu2+
-
5 mM, 86% of initial activity
Cu2+
-
CuCl2, inhibition of glutaminase II
diazo-5-oxo-L-norleucine
-
enzyme from mesenteric lymph nodes
diazo-5-oxo-L-norleucine
-
inactivates dimeric enzyme form in presence or absence of phosphate
dithiothreitol
-
complete inhibition at 1 mM
dithiothreitol
-
5 mM, 82% of initial activity
EDTA
-
80% residual activity at 1 mM
EDTA
-
glutaminase I and II
EDTA
-
10% inhibition at 1 mM
Fe2+
-
0.1 mM, 55% of initial activity
Fe2+
-
92% residual activity at 1 mM
Fe2+
-
5 mM, 83% of initial activity
Fe3+
-
0.1 mM, 45% of initial activity
Fe3+
-
5 mM, 84% of initial activity
glutamate
-
no inhibition
glutamate
-
no inhibition
glutamate
-
inhibits the enzyme in vivo in tumor cells at 100 mM
glutamate
-
competitive with respect to Gln
Hg2+
-
10 mM, 35% of initial activity
Hg2+
-
complete inhibition at 50 mM
Hg2+
-
5 mM, 61% of initial activity
Hg2+
-
0.1 mM, complete inhibition
HgCl2
-
inhibition to a variable extent
iodoacetamide
-
complete inhibition at 50 mM
iodoacetamide
-
5 mM, 3% of initial activity
iodoacetate
-
10 mM, 23% of initial activity
iodoacetate
-
50 mM, strongly inhibited, 80% inhibition, especially more strongly with a progress of purification steps
L-glutamate
-
product inhibition, competitive
L-glutamate
-
strong product inhibition of isozyme KGA, no inhibition of isozyme LGA
L-glutamine
-
product inhibition, strongly inhibits the membrane-associated enzyme, while the soluble form is not or weakly inhibited
L-glutamine
inhibition of enzyme activity in tumor tissue
L-glutamine
Triticale sp.
-
above 0.3 mM
Mersalyl
-
enzyme from mesenteric lymph nodes
Mersalyl
-
0.5 mM, almost complete inhibition
Mersalyl
-
0.5 mM, almost complete inhibition
Mg2+
-
10 mM, 55% of initial activity
Mg2+
-
74.29% residual activity at 100 mM
Mn2+
-
0.1 mM, 75% of initial activity
Mn2+
-
80% residual activity at 1 mM
Mn2+
-
76.23% residual activity at 100 mM
N-ethylmaleimide
-
10 mM, 60% of initial activity
N-ethylmaleimide
-
5 mM, 8% of initial activity
NaCl
-
40% inhibition of the enzyme from strain RIB40 and 90% of the enzyme from strain MA-27-IM at 2.9 M, reduces the temperature stability of the enzyme
NaCl
-
the enzyme activity is inhibited by approximately 95% in the presence of 18% (w/v) NaCl
NaCl
-
enhances activity at 1-20% w/v, but reduces activity by 30% at 25% w/v, at 25% NaCl concentration, the enzyme retains 60% of its activity after 4 h
NaCl
-
15%, remains 90% of the initial activity
NaCl
-
inhibits the enzyme slightly at 2.6 M, the enzyme is salt-tolerant, the C-terminally serine protease-cleaved enzyme fragment shows higher salt tolerance than the full-length enzyme, the N-terminal domain has abundant glutamic acid residues on its surface, which may explain its salt-tolerant mechanism
NEM
-
-
NEM
-
enzyme from mesenteric lymph nodes
NEM
-
enzyme exists as an NEM-sensitive form and an NEM-insensitive form
NEM
-
1 mM, almost completely blocks activity
NEM
-
enzyme exists as an NEM-sensitive form and an NEM-insensitive form
NH3
-
product inhibition, 10 mM inhibits the enzyme activity about 30%
NH4+
-
-
NH4+
-
enzyme from mesenteric lymph nodes
NH4+
Triticale sp.
-
0.01 M, 50% inhibition
p-mercuribenzoate
-
-
p-mercuribenzoate
-
0.1 mM, complete inhibition, presence of Gln prevents inhibition
PCMB
-
inhibition of glutaminase I but not glutaminase II
pyruvate
-
mixed inhibition
pyruvate
-
0.5 M, complete inhibition
Zn2+
-
10 mM, 30% of initial activity
Zn2+
-
82.12% residual activity at 100 mM
Zn2+
-
5 mM, 79% of initial activity
additional information
-
not inhibited by EDTA
-
additional information
-
phenylmethylsulfonyl fluoride, sodium azide, ethylenediaminetetraacetic acid and N-acetylimidazole have no effect on enzyme
-
additional information
-
bis(diphenylarsine)oxide causes no siginficant changes in GAC levels and PAG activities. Methylated inorganic arsenics dimethylarsinic acid, dimethylarsinous acid, and phenyldimethylarsine oxide show no effects on GAC levels and PAG activities. And both glutathione-conjugated diphenylarsinic acid and triphenylarsine had no significant suppressive effects on the GAC levels and PAG activity
-
additional information
-
no inhibition by 2-mercaptomethanol and iodoacetate
-
additional information
-
no inhibition by HgCl2; no inhibition by p-chloromercuribenzoate
-
additional information
no inhibition by HgCl2; no inhibition by p-chloromercuribenzoate
-
additional information
-
no inhibited by glutamate
-
additional information
-
activity is not significantly impaired with 2-oxoglutarate, pyruvate, succinate and citrate, no inhibition with L-glutamate, NH4+ and L-aspartate
-