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1-phenyl-N-[4-(pyridin-2-yl)-1,3-thiazol-2-yl]-1H-imidazole-5-carboxamide
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2'-Phosphoadenosine 5'-phosphosulfate
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2,4,6-Trinitrobenzene sulfonate
2,6-dichlorophenol indophenol
2-(3-fluorophenoxy)-N-[4-(2-pyridyl)thiazol-2-yl]acetamide
shows good docking results. The inhibitor halts not only Entamoeba trophozoite proliferation but also cyst formation
2-(3-fluorophenoxy)-N-[4-(pyridin-2-yl)-1,3-thiazol-2-yl]acetamide
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2-cycloheptyl-4-(4-methoxy-3-[4-[4-(2H-tetrazol-5-yl)phenoxy]butoxy]phenyl)-4a,5,8,8a-tetrahydrophthalazin-1(2H)-one
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2-cycloheptyl-5-(4-methoxy-3-[4-[4-(2H-tetrazol-5-yl)phenoxy]butoxy]phenyl)-4,4-dimethyl-2,4-dihydro-3H-pyrazol-3-one
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3'-phosphoadenosine 5'-phosphosulfate
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product inhibition
3-(methanesulfonyl)-5,7-dimethyl[1,2]thiazolo[3,4-d]pyrimidine-4,6(5H,7H)-dione
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3-phenyl-N-[4-(2-pyridyl)thiazol-2-yl]imidazole-4-carboxamide
shows good docking results. The inhibitor halts not only Entamoeba trophozoite proliferation but also cyst formation
3-[5-(3,5-dichloro-4-fluorophenyl)-5-(trifluoromethyl)-4,5-dihydro-1,2-oxazol-3-yl]-N-[(1-hydroxy-3,3-dimethyl-1,3-dihydro-2,1-benzoxaborol-5-yl)methyl]-5-methylbenzamide
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3-[7-(benzyloxy)-4,8-dimethyl-2-oxo-2H-1-benzopyran-3-yl]propanoic acid
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4-(3-methoxyphenyl)-5-(phenylmethanesulfonyl)-1H-tetrazol-4-ium
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4-Aminophenylacetate
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0.008 mM, 50% inhibition
5-bromo-2-chloro-N-(5-sulfanyl-1,3,4-thiadiazol-2-yl)benzamide
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8-(4-methyl-3-[3-[([2-methyl-5-[(4,6,8-trisulfonaphthalen-1-yl)carbamoyl]phenyl]carbamoyl)amino]benzamido]benzamido)naphthalene-1,3,5-trisulfonic acid
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adenosine 5'-phosphosulfate
adenosine-5'-phosphosulfate
adenylyl sulfate
adenylyl sulfate acts as a strong uncompetitive inhibitor of the APS kinase reaction
ADP
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free form, reverse reaction, weak
ammonium sulfate
high salt inhibits at low adenosine 5'-phosphosulfate concentrations, but activates at high adenosine 5'-phosphosulfate concentrations
auranofin
shows good docking results. The inhibitor halts not only Entamoeba trophozoite proliferation but also cyst formation
Cu2+
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2 mM, 90% inhibition
diethyldicarbonate
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in the presence or absence of ATP-sulfurylase
ferricyanide
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0.05 mM, complete inhibition
iodoacetamide
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strong inhibition, dithiothreitol partially protects
Mn2+
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in excess, activating below
N,N'-[furan-2,5-diylbis(2-chloro-4,1-phenylene)]diguanidine
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N,N'-[furan-2,5-diylbis(3-chloro-4,1-phenylene)]diguanidine
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N-ethylmaleimide
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0.02 mM, 50% inhibition
N-[2-(5-chloro-2-methoxyanilino)-2-oxoethyl]-N-methyl-2-phenyl-2H-1,2,3-triazole-4-carboxamide
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NaClO3
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6.57 mM, 50% inhibition of brain PAPSS activity, 3.26 mM, 50% inhibition of liver PAPSS
p-chloromercuribenzoate
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0.005 mM, 50% inhibition
2,4,6-Trinitrobenzene sulfonate
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0.05 mM, complete inhibition
2,4,6-Trinitrobenzene sulfonate
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in the presence or absence of ATP-sulfurylase
2,4,6-Trinitrobenzene sulfonate
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0.05 mM, 28% inhibition
2,6-dichlorophenol indophenol
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0.05 mM, complete inhibition
2,6-dichlorophenol indophenol
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0.05 mM, complete inhibition
adenosine 5'-phosphosulfate
substrate inhibition above 0.01 mM
adenosine 5'-phosphosulfate
uncompetitive inhibition above 0.001 mM
adenosine 5'-phosphosulfate
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adenosine 5'-phosphosulfate
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adenosine 5'-phosphosulfate
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adenosine 5'-phosphosulfate
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substrate inhibition above 0.03-0.04 mM
adenosine 5'-phosphosulfate
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adenosine 5'-phosphosulfate
substrate inhibition
adenosine 5'-phosphosulfate
acts as a strong uncompetitive inhibitor of the APS kinase reaction
adenosine 5'-phosphosulfate
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adenosine 5'-phosphosulfate
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kinetics
adenosine 5'-phosphosulfate
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adenosine 5'-phosphosulfate
adenosine 5'-phosphosulfate can bind to E-MgADP forming a catalytically inactive E-MgADP-APS ternary complex
adenosine 5'-phosphosulfate
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potent substrate inhibition, ATP reverses
adenosine 5'-phosphosulfate
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adenosine-5'-phosphosulfate
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adenosine-5'-phosphosulfate
substrate inhibition
adenosine-5'-phosphosulfate
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substrate inhibition
ATP
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in the absence of ATP regenerating system, substrate inhibition above 0.6 mM, in the presence of ATP regenerating system, substrate inhibition above 0.2 mM
ATP
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free form, weak inhibition; MgATP2-: product inhibition, reverse reaction
ATP
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inhibition by free ATP, i.e. in excess of total Mg2+
Bromosuccinimide
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strong inhibition
Bromosuccinimide
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0.05 mM, complete inhibition
Bromosuccinimide
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0.05 mM, complete inhibition
Co2+
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2 mM, 63% inhibition
Co2+
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in excess, activating below
dehydroascorbate
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EDTA
complete inhibition
FAD
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GSSG
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Mercuriphenylacetate
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0.05 mM, complete inhibition
Mercuriphenylacetate
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0.05 mM, complete inhibition
oxidized glutathione
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thioredoxin reverses inactivation
additional information
validation of in silico molecular docking analysis and an in vitro enzyme activity assay for large scale screening. Inhibitor screening, In silico molecular docking analysis and simulation ranks the binding free energy between a homology modeling structure of EhAPSK and 400 compounds, overview. Analysis of the cytotoxicity
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additional information
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validation of in silico molecular docking analysis and an in vitro enzyme activity assay for large scale screening. Inhibitor screening, In silico molecular docking analysis and simulation ranks the binding free energy between a homology modeling structure of EhAPSK and 400 compounds, overview. Analysis of the cytotoxicity
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additional information
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not inhibited by Mg2+
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additional information
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additional information
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not inhibited by adenosine 5'-phosphosulfate
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additional information
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not inhibited by ferricyanide
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additional information
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additional information
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not inhibited by ATP
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