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(2E,6E)-2,6-bis[(thiophen-2-yl)methylidene]cyclohexan-1-one
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(E)-([[5-(5-bromothiophen-2-yl)-1,3-thiazol-2-yl]amino]methylidene)amino 4-nitrobenzoate
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1,3-dichloro-2-(4-nitrophenoxy)benzene
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1-(2,6-dimethylphenyl)-3-thiophen-2-ylurea
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1-(3-chloro-4-fluoro-phenyl)-3-(3-chloro-phenyl)-urea
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1-(3-chloro-4-fluorophenyl)-3-[3-(4-chlorophenyl)-4-cyano-5-(methylsulfanyl)thiophen-2-yl]urea
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1-[3-[([[(4Z)-3,4-dihydro-1H-2-benzothiopyran-4-ylidene]amino]oxy)methyl]-4-methoxyphenyl]ethan-1-one
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1-[5-(4-chloro-benzylsulfanyl)-[1,3,4]thiadiazol-2-yl]-3-(4-chloro-phenyl)-urea
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2',5'-ATP-ribose
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competitive inhibition, competitive in forming complexes with reductase
2-(4-bromothiophen-2-yl)-1,3-dithiolane
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2-(benzylamino)-2-(3,4-dichlorophenyl)acetonitrile
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2-(benzylsulfanyl)-5-chloro-1,3-benzothiazole
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2-([2-[(2-aminophenyl)sulfanyl]-6-nitro-4-(trifluoromethyl)phenyl]sulfanyl)aniline
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2-amino-4-(4-chlorophenyl)-9-fluoro-4H,5H-pyrano[3,2-c]chromene-3-carbonitrile
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2-chloro-6H-5-thia-7-azatetraphene-12-carboxylic acid
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2-oxo-2-phenylethyl 3-iodobenzoate
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2-phenyl-1,2-benzoselenazol-3-one
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2-[4-(4-chlorophenyl)-2H-1,3-dithiol-2-ylidene]propanedinitrile
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3,5-diethyl 4-[5-[2-chloro-5-(trifluoromethyl)phenyl]furan-2-yl]-2,6-dimethyl-1,4-dihydropyridine-3,5-dicarboxylate
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3-(1-ethynylcyclohexyl)-1-(6-[[(1-ethynylcyclohexyl)carbamoyl]amino]hexyl)urea
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3-(3-chlorophenyl)-1-[2-(thiophene-2-sulfonamido)phenyl]urea
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3-(3-chlorophenyl)-4-cyano-5-(methylsulfanyl)thiophene-2-carboxylic acid
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3-(5-methyl-2-oxo-2,3-dihydro-1,3-benzoxazol-3-yl)-N'-[3-(thiophen-2-yl)-1,2,4-oxadiazole-5-carbonyl]propanehydrazide
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3-amino-5-[(cyanomethyl)sulfanyl]-4-(propane-2-sulfonyl)thiophene-2-carbonitrile
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3-[3-[(2,4-dichlorophenyl)sulfanyl]-3-oxopropyl]-2,3-dihydro-1,3-benzoxazol-2-one
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4-(1,3-dithiolan-2-yl)-2-methoxy-6-nitrophenyl 2,5-dichlorobenzene-1-sulfonate
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4-(2-fluorophenyl)-N,N-bis(propan-2-yl)benzamide
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4-(4-chlorobenzenesulfonyl)-N-(2,4-difluorophenyl)-3-methylthiophene-2-carboxamide
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4-amino-3,5-dichloro-N-(2,4,5-trichlorophenyl)benzamide
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4-bromo-3-[(1E)-[2-(2,4-dichlorophenyl)hydrazin-1-ylidene]methyl]-1-methyl-1H-pyrazole
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4-cyclohexyl-2-[[(2,5-dimethylphenyl)methyl]sulfanyl]-6-oxo-1,6-dihydropyrimidine-5-carbonitrile
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5-methyl-4-phenyl-N-([[3-(trifluoromethyl)phenyl]carbamoyl]amino)-1,3-oxazole-2-carboxamide
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adenosine 2',5'-diphosphate
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benzalkonium chloride
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benzethonium chloride
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Butanedione
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inhibitor of transhydrogenase and diaphorase activity, reacts with arginine residue involved in binding of pyridine nucleotides
diphosphate
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inhibitor of ferredoxin-dependent photoreduction
disulfodisalicylidenepropane-1,1-diamine
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inhibits all reactions except photoreduction of cytochrome c
ethyl 2-[3-(3,4,5-trimethoxyphenyl)propanamido]acetate
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ethyl 5-benzamido-4-cyano-3-methyl-1-phenyl-1H-pyrrole-2-carboxylate
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flavodoxinI/II
inhibition of electron transfer at higher electron acceptor rate
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guanidine hydrochloride
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0.1 M guanidine hydrochloride reduces activity by 30%, 0.2 M guanidine hydrochloride by 60%, and 0.4 M guanidine hydrochloride by 85%, concentrations over 0.7 M guanidine hydrochloride eliminate activity
heparin
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binds to the enzyme, inhibits ferredoxin and NADPH binding to the enzyme
methyl 3-[2-(thiophen-2-yl)acetamido]thiophene-2-carboxylate
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Mg2+
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inhibits reduction of plastoquinone incorporated into sodium cholate micelles
MgCl2
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inhibits at lower salt concentrations
myristyltrimethylammonium bromide
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inhibits reduction of plastoquinone almost completely at 15 mM
N-(2-[[3-cyano-6-methyl-5-(2-methyl-1,3-thiazol-4-yl)pyridin-2-yl]sulfanyl]ethyl)-3-(trifluoromethyl)benzene-1-sulfonamide
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N-(2H-1,3-benzodioxol-5-yl)-4,6-dimethyl-1H-indole-2-carboxamide
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N-(4-butyl-2-methylphenyl)-2-[(5-cyano-4-cyclohexyl-6-oxo-1,6-dihydropyrimidin-2-yl)sulfanyl]acetamide
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N-ethyl-3(3-dimethylaminopropyl)carbodiimide
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N-[2-[3-(4-chlorophenyl)-1,2,4-oxadiazol-5-yl]phenyl]-2,2,2-trifluoroacetamide
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N-[3,5-bis(trifluoromethyl)phenyl]-2-[(5-chloro-1,3-benzoxazol-2-yl)sulfanyl]acetamide
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N-[3-(4-chlorophenyl)-4-cyano-5-(methylsulfanyl)thiophen-2-yl]morpholine-4-carboxamide
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N-[4-cyano-5-(methylthio)-2-thienyl]-N'-[3-(trifluoromethyl)phenyl]urea
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N6-(6-aminohexyl)-2',5'-ADP
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competitive inhibition
NADPH
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reversible inhibition, is turned to irreversible in presence of 4 M urea
octylglucoside
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inhibits reduction of plastoquinone
oxidized ferredoxin
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inhibits binding of reduced ferredoxin and reduction of flavin
SDS
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inhibits reduction of plastoquinone almost completely at 15 mM
Triton X-100
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inhibits reduction of plastoquinone
Urea
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1 M urea reduces activity by 20%, 2 M urea by 40%, and 3 M urea by 80%, concentrations over 5 M urea eliminate activity
[Cr[CN]6]4-
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binds to the enzyme
2',5'-ADP
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competitive inhibition
2',5'-ADP
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competitive inhibition, but there could also be a non-competitive component caused by binding at a weak secondary NADP+ binding site
2'-AMP
when 2,6-dichlorophenolindophenol serves as electron acceptor
Cd2+
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70% inhibition, uncompetitive to dibromothymoquinone, noncompetitive inhibition of NADPH oxidation, Zn2+ diminishes the inhibitory effect for dibromothymoquinone reduction, but enhances inhibition of ferricyanide reduction, inhibitory effect on ferricyanide reduction, but on dibromothymoquinone reduction, is abolished by addition of 2-mercaptoethanol or histidine, inhibition mechnanism, overview
Cd2+
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noncompetitive type of inhibition, effect of cadmium binding is significant disturbance in the electron transfer process from FAD to dibromothymoqinone, but less interference with the reduction of ferricyanide. It causes a strong inhibition of ferredoxin reduction, indicating that Cd-induced changes in the FNR structure disrupt ferredoxin binding. Iodoacetamide blocks the sensitivity to Cd2+ inhibition. pH-Dependent inhibition: to interact with cadmium in a mode which leads to inhibition, the cysteine residues of FNR have to be charged. Almost no inhibition in pH lower than pH 7.7, while in pH higher than pH 8.1 the reduction of activity caused by cadmium ions increases, FNR cysteine-peptide mapping, overview. Triticum aestivum FNR is more sensitive to lower cadmium concentrations than the Spinacia oleracea enzyme
Cd2+
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noncompetitive type of inhibition, effect of cadmium binding is significant disturbance in the electron transfer process from FAD to dibromothymoqinone, but less interference with the reduction of ferricyanide. It causes a strong inhibition of ferredoxin reduction, indicating that Cd-induced changes in the FNR structure disrupt ferredoxin binding. Iodoacetamide blocks the sensitivity to Cd2+ inhibition. pH-Dependent inhibition: to interact with cadmium in a mode which leads to inhibition, the cysteine residues of FNR have to be charged. Almost no inhibition in pH lower than pH 7.7, while in pH higher than pH 8.1 the reduction of activity caused by cadmium ions increases, FNR cysteine-peptide mapping, overview. Triticum aestivum FNR is more sensitive to lower cadmium concentrations than the Spinacia oleracea enzyme
Ferredoxin
inhibition of electron transfer at higher electron acceptor rate
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Ferredoxin
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oxidized ferredoxin inhibits both the first and second one-electron reduction
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Ferredoxin
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competitive inhibitor with NADPH in dichlorophenolindophenol reductase reaction
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iodoacetamide
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NaCl
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ferredoxin-dependent activity decreases with increasing NaCl concentration and disappears at concentrations over 0.5 M NaCl
NaCl
ferredoxin-dependent activity decreases with increasing NaCl concentration and disappears at concentrations over 0.5 M NaCl
NaCl
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high concentration
rubredoxin
substrate inhibition is observed with electron donor NADPH
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rubredoxin
substrate inhibition is observed with electron donor NADPH, but not with NADH
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Triazine dyes
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interaction with the enzyme, competitive inhibitor of NADPH in ferricyanide reduction assays
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Triazine dyes
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competitive inhibition of diaphorase activity
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additional information
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activity decreases with elevated ionic strength
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additional information
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enzyme is activated by light and inactivated by dark
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additional information
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FNR is inactivated after prolonged dark exposure
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additional information
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induction of FprB expression is not affected by oxidative stress agents, such as paraquat, menadione, H2O2, and t-butyl hydroperoxide
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additional information
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association of ferredoxin inhibits binding of NADPH
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additional information
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histidine and 2-mercaptoethanol are not inhibitory
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additional information
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gradual decrease in activity according to biphasic kinetics within 120 min, 80% of maximal activity can be restored by addition of DTNB or fluoresamine, dibromothymoquinone influences the inhibitory pattern and modifies the enzyme conformation
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additional information
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inhibited by specific antibodies
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