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(1H-indol-1-yl)(furan-2-yl)methanone
noncompetitive inhibitor
(1H-indol-1-yl)(tiyophen-2-yl)methanone
competitive inhibitor
(2R,3R)-2-(3,4-dihydroxyphenyl)-5,7-dihydroxy-3,4-dihydro-2H-chromen-3-yl 3,4,5-trihydroxybenzoate
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(2R,3R)-5,7-dihydroxy-2-(3,4,5-trihydroxyphenyl)-3,4-dihydro-2H-chromen-3-yl 3,4,5-trihydroxybenzoate
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(2S,3R)-2-(3,4-dihydroxyphenyl)-5,7-dihydroxy-3,4-dihydro-2H-chromen-3-yl 3,4,5-trihydroxybenzoate
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(2S,3R)-5,7-dihydroxy-2-(3,4,5-trihydroxyphenyl)-3,4-dihydro-2H-chromen-3-yl 3,4,5-trihydroxybenzoate
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(3alpha)-3,21-dihydroxypregnan-20-one
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(4Z)-4-(3-bromobenzylidene)-1-(4-methylphenyl)pyrazolidine-3,5-dione
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(5Z)-1-(4-bromophenyl)-5-[[5-(2-nitrophenyl)furan-2-yl]methylidene]pyrimidine-2,4,6(1H,3H,5H)-trione
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(5Z)-1-(4-ethoxyphenyl)-5-[[5-(2-nitrophenyl)furan-2-yl]methylidene]pyrimidine-2,4,6(1H,3H,5H)-trione
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(5Z)-5-[[5-(2-methyl-4-nitrophenyl)furan-2-yl]methylidene]-1-(3-methylphenyl)pyrimidine-2,4,6(1H,3H,5H)-trione
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reversible, non-competitive inhibition versus NADP+, mixed-type versus D-glucose 6-phosphate
1-(2-nitro-1-(thiophen-2-yl)ethyl)-1H-indole
competitive inhibitor
16-bromoepiandrosterone
no activity at 0.03 mM
2'-phosphoadenosine 5'-diphosphoribose
-
-
2,3-diphosphoglycerate
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2-[(5Z)-5-(4-hydroxy-3-methoxybenzylidene)-4-oxo-2-thioxo-1,3-thiazolidin-3-yl]-3-phenylpropanoate
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2-[(E)-(4-nitrocyclohexa-2,4-dien-1-yl)(2-phenylhydrazinylidene)methyl]benzene-1,4-diol
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non-competitive inhibition versus NADP+, non-competitive or mixed-type versus D-glucose 6-phosphate
2-[4-(4-chlorophenyl)-1,3-thiazol-2-yl]-5-methyl-4-(3,4,5-trimethoxybenzyl)-2,4-dihydro-3H-pyrazol-3-one
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irreversible, non-competitive inhibition versus NADP+, mixed-type versus D-glucose 6-phosphate
3-(3,4-dichlorophenyl)-1,1'-dimethyl urea
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cytosolic isozyme, inhibition by uncoupling of photosynthetic electron transport
3-(4-hydroxyphenyl)-2-(pyridin-3-yl)quinazolin-4(3H)-one
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irreversible, non-competitive inhibition versus NADP+, mixed-type versus D-glucose 6-phosphate
3-(5-bromopyridin-2-yl)-2-(pyridin-3-yl)quinazolin-4(3H)-one
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irreversible, non-competitive inhibition versus NADP+, mixed-type versus D-glucose 6-phosphate
3-(5-[(E)-[2-(5-nitropyridin-2-yl)hydrazinylidene]methyl]furan-2-yl)benzoic acid
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4-fluoro-N-(4-hydroxynaphthalen-1-yl)benzenesulfonamide
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4-methyl-3-(propan-2-yloxy)-6H-benzo[c]chromen-6-one
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non-competitive inhibition versus NADP+, mixed-type versus D-glucose 6-phosphate
5-(3alpha,7alpha,12alpha-triacetoxy-5-beta-cholanamido)-1,3,4-thiadiazole-2-sulfonamide
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weak inhibition
5-(3alpha,7alpha,12alpha-trihydroxy-5-beta-cholanamido)-1,3,4-thiadiazole-2-sulfonamide
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weak inhibition
5-[[5-(4-methoxy-2-nitrophenyl)furan-2-yl]methylidene]-2-thioxodihydropyrimidine-4,6(1H,5H)-dione
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reversible, competitive inhibition versus NADP+, mixed-type versus D-glucose 6-phosphate
5alpha-androstan-16-alpha-bromo-3beta-ol-17-one
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in vitro cell viability assays shows a LD50 of 20 microM for Trypanosoma cruzi epimastigotes
5alpha-Androstan-3beta-ol-17-one
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uncompetitive inhibitor
5alpha-androsten-16-alpha-bromo-3beta-ol-17-one
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potent inhibitor, in vitro cell viability assays shows a LD50 of 12 microM for Trypanosoma cruzi epimastigotes
6-amino-NAD+
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irreversibly inhibits G6PD
6-amino-NADP+
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irreversibly inhibits G6PD
adenosine 5' [beta,gamma-amido] triphosphate
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adenosine 5' [beta-thio] diphosphate
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adenosine 5' [gamma-thio] triphosphate
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amikacin
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in vitro, noncompetitive
ammonia
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inhibition in vitro and in vivo at sublethal concentration of 0.0022-0.0055 mM, IC50: 0.0187 mM
beta-naphthoquinone-4-sulfonic acid
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1 mM, 68% inhibition, G6PDH-1; 1 mM, 81% inhibition, G6PDH-2
brimonidine
competitive inhibition
Ca2+
-
about 90% residual activity at 2 mM
ceftriaxone
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strongly inhibits
cumene hydroperoxide
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1% residual activity after treatment with 17 mM cumene hydroperoxide at 50°C and pH 7 for 2 h
cypermethrin
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inhibits G6PD in vitro
dehydroandrosterone
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uncompetitive inhibitor
deltamethrin
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inhibits G6PD both in vivo and in vitro, significantly inhibits activity after the 48th hour. Among pesticides, it is the most effective one, which is widely used both at homes and in agricultural fields. Deltamethrin inhibits the enzyme at very low doses, particularly in in vivo conditions, indicating that fish in natural and cultural environments are susceptible to this pesticide and that deltamethrin contaminations can be cause high mortality in fish population, which may lead to the increase in food insufficiency for increasing populations and cause disruption of ecological balance. Thus, usage of deltamethrin must be well controlled
dithiothreitol
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about 40% inhibition at 5 mM
ellagic acid
mixed type inhibitor of glucose 6-phosphate activity
gentamicin sulfate
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in vitro, noncompetitive
glyceraldehyde 3-phosphate
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-
guanidinium hydrochloride
guanosine hydrochloride
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the enzyme shows a sharp loss in activity above 0.75 M, but is activated by low concentrations of 0.2 M of GdmCl
hydrogen peroxide
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inhibitory at 0.25%, at pH 7
lidocaine
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strongly inhibits
marcaine
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noncompetitive
meloksikam
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strongly inhibits
N-(4-chlorobenzoyl)-indole
competitive inhibitor
N-(4-hydroxynaphthalen-1-yl)-2,5-dimethylbenzenesulfonamide
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-
N-benzoylindole
noncompetitive inhibitor
N-ethyl-N'-[(3alpha)-17-oxoandrostan-3-yl]urea
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N-[(3alpha)-17-oxoandrostan-3-yl]sulfuric diamide
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N-[(3alpha)-21-hydroxy-20-oxopregnan-3-yl]sulfuric diamide
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netilmicin
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inhibition of wild-type and mutant enzymes 1-3
Ni2+
-
about 95% residual activity at 2 mM
Nicotine
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inhibits the enzyme from lung, testis, kidney, stomach, and brain, in concert with vitamin E the enzyme from testis brain and liver is inhibited, tissue-specific inhibition of 12.5-48%, overview, nicotine has no effect on enzyme from muscle, heart, and liver
oleic acid
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G6PDH-1 is more susceptible to oleic acid than G6PDH-2
Pb2+
-
noncompetitive inhibition
penicillin G potassium
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in vitro, noncompetitive
pental sodium
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noncompetitive
peracetic acid
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1% residual activity after treatment with 4 mM peracetic acid at 25°C and pH 7 for 15 min
phenylmethylsulfonyl fluoride
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about 48% inhibition at 5 mM
phosphoenol pyruvate
-
25% inhibition at 10 mM
prilocaine
-
strongly inhibits
propoxur
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inhibits G6PD in vitro
pyridoxal 5'-phosphate
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-
quartz
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24 h incubation with quartz particles (80 microg/cm(2)) inhibits G6PD activity by 70%. Inhibition is fully prevented by glutathione. Silica exerts on G6PD an oxidative damage
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Ribulose 1,5-diphosphate
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sodium ceftizoxime
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inhibition of wild-type and mutant enzymes 1-3
sodium cefuroxime
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inhibition of wild-type and mutant enzymes 1-3
streptomycin
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inhibition of wild-type and mutant enzyme 3
suramin
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77% inhibition at 0.05 mM
tert-butyl hydroperoxide
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1% residual activity after treatment with 290 mM tert-butyl hydroperoxide at 50°C and pH 7 for 3 h
Thioredoxin f
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from chloroplasts
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Tl+
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201Tl solution and radiation exposure has inhibitory effects on the enzyme activity both in vivo and in vitro
Trypsin
after 2 h of trypsin digestion in the presence of 0.01 mM NADP+ the enzyme retains about 57% of its original activity
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Urea
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inhibition in vitro and in vivo at sublethal concentration of 0.02-0.05 mM, IC50: 0.0238 mM
vitamin E
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in concert with nicotine the enzyme from testis brain and liver is inhibited, while the enzyme from muscle and stomach is activated, overview
ADP
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ADP
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15% inhibition at 2 mM
ADP
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about 65% inhibition at 5 mM
AMP
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5% inhibition at 2 mM
ATP
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-
ATP
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31% inhibition at 5 mM, non-competitive inhibition with respect to D-glucose 6-phosphate
ATP
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2.0 mM, 65% inhibition, G6PDH-2; G6PDH-1
ATP
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10 mM, 50-75% inhibition, assay without MgCl2
ATP
-
weak, noncompetitive inhibition
ATP
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15% inhibition at 2.5 mM, 24% inhibition at 10 mM
Cd2+
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-
Cd2+
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1 mM, 53% inhibition, G6PDH-1
Cd2+
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1 mM, 83% inhibition
Cd2+
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noncompetitive inhibition
Co2+
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competitive, 60% inhibition at 0.01 mM
Co2+
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1 mM, 56% inhibition
Cu2+
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potent inhibitor, about 65% residual activity at 2 mM (isoform G6PD2), about 50% residual activity at 2 mM (isoform G6PD1)
Cu2+
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about 15% residual activity at 5 mM
Cu2+
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1 mM, 24% inhibition, G6PDH-1; 1 mM, 78% inhibition, G6PDH-2
Cu2+
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1 mM, complete inhibition
Cu2+
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noncompetitive inhibition
D-glucose 6-phosphate
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about 48% inhibition at 5 mM
D-glucose 6-phosphate
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-
dehydroepiandrosterone
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non-competitively inhibits
dehydroepiandrosterone
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uncompetitively inhibits bloodstream form cells
DTT
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DTT
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1 mM, 2 h, 20% loss of activity in the first 15 min and then the enzyme activity remains steady throughout the incubation
EDTA
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5 mM, 85% inhibition, G6PDH-1; 5 mM, 97% inhibition, G6PDH-2
epiandrosterone
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non-competitively inhibits
epiandrosterone
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uncompetitively inhibits bloodstream form cells
epiandrosterone
uncompetitive inhibitor, 12% residual activity at 0.03 mM
Fe2+
-
potent inhibitor, about 10% residual activity at 5 mM (isoform G6PD2), about 30% residual activity at 5 mM (isoform G6PD1)
Fe2+
-
about 30% residual activity at 5 mM
Fe2+
-
strong competitive inhibition
Fe3+
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enzyme activities are significantly decreased in the presence of 30 and 300 ppm Fe3+
Fe3+
competitive inhibitor against the G6PD enzyme with respect to NADP+ and D-glucose 6-phosphate
glucosamine 6-phosphate
-
competitive G6PDH inhibitor
glucosamine 6-phosphate
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parabolic inhibition
glucose
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at concentration above 10 mM
glucose
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high glucose level of 25 mM leads to a decrease in G6PD activity and protein level in islets
GTP
-
-
guanidinium hydrochloride
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denatures
guanidinium hydrochloride
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in the presence of 4 M, after 2 hours all secondary structure is lost
Hg2+
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1 mM, 47% inhibition, G6PDH-2; 1 mM, 84% inhibition, G6PDH-1
Hg2+
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1 mM, complete inhibition
Hg2+
-
noncompetitive inhibition
metamizol
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strongly inhibits
metamizol
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inhibition of wild-type and mutant enzyme 3
Mn2+
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about 10% residual activity at 5 mM (isoform G6PD2)
Mn2+
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1 mM, 56% inhibition
NADH
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about 38% inhibition at 5 mM
NADH
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allosteric inhibition, inhibition is not reversed by NAD+, AMP, or spermidine
NADP+
-
substrate inhibition
NADP+
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at concentrations above 0.3 mM
NADP+
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at high concentration, dead-end ternary complexes are formed
NADPH
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-
NADPH
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product inhibition
NADPH
-
competitive inhibition
NADPH
-
competitive inhibition with respect to NADP+ and D-glucose 6-phosphate
NADPH
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about 90% inhibition at 0.2 mM
NADPH
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has a regulatory role in pentaose phosphate pathway
NADPH
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product inhibition with NADP+ or D-glucose 6-phosphate as the varying substrate
NADPH
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when NADP+ is the varied substrate, NADPH NADPH is a competitive inhibitor both in the presence and absence of Mg2+, linear competitive inhibition. When glucose 6-phosphate is the varied substrate NADPH causes linear noncompetitive inhibition
NADPH
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NADPH binding is important for physiological regulation of pentose phosphate pathway
NADPH
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slight inhibition
NADPH
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inhibition patterns of substrates and product
NADPH
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liver enzyme is more sensitive to inhibition than kidney enzyme
p-chloromercuribenzoate
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-
p-chloromercuribenzoate
-
can be reversed 100% by dithiothreitol, partially by glutathione
p-chloromercuribenzoate
-
-
palmitoyl-CoA
-
-
palmitoyl-CoA
-
non-competitive
palmitoyl-CoA
-
leads to dissociation of active tetramers to inactive dimers
palmitoyl-CoA
-
leads to dissociation of active tetramers to inactive dimers
phosphoenolpyruvate
-
-
phosphoenolpyruvate
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13% inhibition at 2.5 mM, 31% inhibition at 10 mM
RNAi
-
suppression of endogenous cytosolic G6PDH isoforms result in highly uniform defense responses and also enhanced drought tolerance and flowering
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RNAi
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mediates reduction of the G6PDH level in bloodstream form cells
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Vancomycin
-
-
Zn2+
-
competitive, 40% inhibition at 0.01 mM
Zn2+
-
potent inhibitor, about 58% residual activity at 5 mM (isoform G6PD2), about 35% residual activity at 2 mM (isoform G6PD1)
Zn2+
-
about 50% residual activity at 5 mM
Zn2+
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1 mM, 83% inhibition, G6PDH-2; 1 mM, 94% inhibition, G6PDH-1
Zn2+
-
noncompetitive inhibition
additional information
Trx f1 regulates G6PDH1 activity as efficiently as Trx m1 or m4. Trx x is a very poor regulator of G6PDH activity. Trx y1 is inefficient as inhibitor but it shows high efficiency in activation. Upon illumination, a strong and fast reductive inhibition of G6PDH1 activity dependent on the presence of all the components of the Fd/Trx system
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additional information
during 7 days of phosphate starvation, G6PD5 is continuously expressed throughout phosphate-starvation; during 7 days of phosphate starvation, transcript levels are reduced; during 7 days of phosphate starvation, transcript levels are reduced; during 7 days of phosphate starvation, transcript levels are reduced; during 7 days of phosphate starvation, transcript levels are reduced; during 7 days of phosphate starvation, transcript levels are reduced
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additional information
during 7 days of phosphate starvation, G6PD5 is continuously expressed throughout phosphate-starvation; during 7 days of phosphate starvation, transcript levels are reduced; during 7 days of phosphate starvation, transcript levels are reduced; during 7 days of phosphate starvation, transcript levels are reduced; during 7 days of phosphate starvation, transcript levels are reduced; during 7 days of phosphate starvation, transcript levels are reduced
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additional information
during 7 days of phosphate starvation, G6PD5 is continuously expressed throughout phosphate-starvation; during 7 days of phosphate starvation, transcript levels are reduced; during 7 days of phosphate starvation, transcript levels are reduced; during 7 days of phosphate starvation, transcript levels are reduced; during 7 days of phosphate starvation, transcript levels are reduced; during 7 days of phosphate starvation, transcript levels are reduced
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additional information
during 7 days of phosphate starvation, G6PD5 is continuously expressed throughout phosphate-starvation; during 7 days of phosphate starvation, transcript levels are reduced; during 7 days of phosphate starvation, transcript levels are reduced; during 7 days of phosphate starvation, transcript levels are reduced; during 7 days of phosphate starvation, transcript levels are reduced; during 7 days of phosphate starvation, transcript levels are reduced
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additional information
during 7 days of phosphate starvation, G6PD5 is continuously expressed throughout phosphate-starvation; during 7 days of phosphate starvation, transcript levels are reduced; during 7 days of phosphate starvation, transcript levels are reduced; during 7 days of phosphate starvation, transcript levels are reduced; during 7 days of phosphate starvation, transcript levels are reduced; during 7 days of phosphate starvation, transcript levels are reduced
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additional information
during 7 days of phosphate starvation, G6PD5 is continuously expressed throughout phosphate-starvation; during 7 days of phosphate starvation, transcript levels are reduced; during 7 days of phosphate starvation, transcript levels are reduced; during 7 days of phosphate starvation, transcript levels are reduced; during 7 days of phosphate starvation, transcript levels are reduced; during 7 days of phosphate starvation, transcript levels are reduced
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additional information
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during 7 days of phosphate starvation, G6PD5 is continuously expressed throughout phosphate-starvation; during 7 days of phosphate starvation, transcript levels are reduced; during 7 days of phosphate starvation, transcript levels are reduced; during 7 days of phosphate starvation, transcript levels are reduced; during 7 days of phosphate starvation, transcript levels are reduced; during 7 days of phosphate starvation, transcript levels are reduced
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additional information
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product and dead-end inhibition studies, overview, no inhibition by AMP
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additional information
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less than 8% inhibition with 1,10-phenanthroline, ATP, EDTA, and iodoacetamide. Not inhibited by NAD+
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additional information
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NADH: no inhibition at up to 0.5 mM
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additional information
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hyperaldosteronism downregulates G6PD and whereby decreases GSH levels and conversely increases oxidative stress, which evokes endothelial-derived NO and impairs vascular function
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additional information
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fluoride-containing bioactive glasses as used in tissue engineering as well as bone repair, inhibit the pentose phosphate oxidative pathway and the glucose 6-phosphate dehydrogenase activity. The effects are ascribable to the fluoride content/release of glass powders, they are mimicked by NaF solutions and are prevented by radical scavengers dimethyl sulfoxide and tempol, by superoxide dismutase, and by glutathione, but not by apocynin
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additional information
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non-radioactive Tl+, Fe3+ and Cu2+ do not influence the enzyme in vitro
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additional information
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is not inhibited by dehydroepiandrosterone and epiandrosterone
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additional information
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effects of streptomycin sulfate and tetracyclin antibiotics
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additional information
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high-throughput screening for small-molecule inhibitors of the enzyme from Plasmodium falciparum, inhibitor evaluation, structure-activity relationship analysis, overview
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additional information
presence of H2O2 only slightly alters enzyme activity or expression
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additional information
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presence of H2O2 only slightly alters enzyme activity or expression
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additional information
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not inhibited by ATP, phosphate, or Mg2+
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additional information
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inhibition of G6PD protects rat hearts from ischemia-reperfusion injury induced by oxidative stress
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additional information
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the cytosolic isoyzme is not affected by osmotic change, phosphate sequestration, or ocidative stress
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