2.3.2.8: arginyltransferase
This is an abbreviated version!
For detailed information about arginyltransferase, go to the full flat file.
Word Map on EC 2.3.2.8
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2.3.2.8
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arginylation
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2.5.1.18
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rx:glutathione
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rx
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n-degrons
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polyubiquitylates
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medicine
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agriculture
- 2.3.2.8
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arginylation
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2.5.1.18
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rx:glutathione
- rx
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n-degrons
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polyubiquitylates
- medicine
- agriculture
Reaction
Synonyms
Arg-transferase, Arg-tRNA transferase, Arg-tRNA-protein transferase, Arg-tRNA-proteintransferase, arginyl transferase, arginyl tRNA transferase, arginyl-transfer ribonucleate-protein aminoacyltransferase, arginyl-transfer ribonucleate-protein transferase, arginyl-transferase, arginyl-tRNA protein transferase, arginyl-tRNA--protein transferase, arginyl-tRNA--protein transferase 1, arginyl-tRNA-protein transferase, arginyl-tRNA-protein transferase 1, arginyl-tRNA:protein arginyltransferase, arginyltransferase, arginyltransferase 1, ATE, Ate1, ATE1-1, ATE1-2, Ate1-3, Ate1-4, ATE1-encoded R-transferase, DdAte1, L-arginyltransferase, R-transferase
ECTree
2.3.2.8 arginyltransferaseAdvanced search results
results (
results (Inhibitors
Inhibitors on EC 2.3.2.8 - arginyltransferase
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INHIBITOR 
ORGANISM
UNIPROT
COMMENTARY 
LITERATURE
IMAGE
homocysteine-responsive endoplasmic reticlulum protein
i.e. HERP, a key inhibitor of the turnover and N-terminal arginylation of molecular chaperone BiP. HERP is a 43-kDa endoplasmic reticlulum (ER) membrane-integrated protein that is an essential component of ER-associated protein degradation
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p-[(bromoacetyl)amino]phenylarsenoxide
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irreversible, potent inhibitor
phenylarsenoxide
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inhibition below 0.005 mM is fully reversed by excess dithiothreitol
Di- and tripeptides
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with glutamyl-, asparagyl- and to a lesser extent cystinyl-NH2-terminal residues, competitive to bovine serum albumin acceptor
Di- and tripeptides
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most potent inhibitor is Glu-Val-Phe, inhibits transfer of arginine to acceptor proteins
hemin
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Fe3+-heme, inhibits arginyl-transferase through a redox mechanism that involves the formation of disulfide between the enzymes Cys-71 and Cys-72 residues
hemin
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Fe3+-heme, inhibits arginyl-transferase through a redox mechanism that involves the formation of disulfide between the enzymes Cys-71 and Cys-72 residues
heparin
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50% inhibition at 0.05 mg/ml, kinetics, competitive to L-arginyl-tRNA
heparin
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50% inhibition at 0.05 mg/ml, kinetics, competitive to L-arginyl-tRNA
additional information
para-chloroamphetamine, PCA, a specific inhibitor of the arginylation branch of the pathway (Arg/N-end rule pathway). PCA significantly alters various biological pathways, including cellular responses to stress, nutrient, and DNA damage, which are also closely involved in modulation of autophagic responses. Treatment with para-chloroamphetamine (PCA) delays the fusion of autophagosomes with lysosomes and leads to the accumulation of autophagic markers. Analysis of PCA effects in wild-type and mutant (ubr1-/- ubr2-/-) HeLa cells. The direct targets of PCA are UBR1 and UBR2 proteins, not ATE1, an upstream component of the Arg/N-end rule pathway
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additional information
para-chloroamphetamine, PCA, a specific inhibitor of the arginylation branch of the pathway (Arg/N-end rule pathway). PCA significantly alters various biological pathways, including cellular responses to stress, nutrient, and DNA damage, which are also closely involved in modulation of autophagic responses. Treatment with para-chloroamphetamine (PCA) delays the fusion of autophagosomes with lysosomes and leads to the accumulation of autophagic markers. Analysis of PCA effects in wild-type and mutant (ubr1-/- ubr2-/-) MEFs. The direct targets of PCA are UBR1 and UBR2 proteins, not ATE1, an upstream component of the Arg/N-end rule pathway
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additional information
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no inhibition by chondroitinsulfate A, B or C, hyaluronic acid, D-glucosamine N-sulfate, D-glucose 6-sulfate, D-glucosamine, D-galactosamine, N-acetyl-D-glucosamine, N-acetyl-D-galactosamine, D-xylose, D-glucuronic acid
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additional information
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no inhibition by chondroitinsulfate A, B or C, hyaluronic acid, D-glucosamine N-sulfate, D-glucose 6-sulfate, D-glucosamine, D-galactosamine, N-acetyl-D-glucosamine, N-acetyl-D-galactosamine, D-xylose, D-glucuronic acid
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additional information
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no inhibition by chondroitinsulfate A, B or C, hyaluronic acid, D-glucosamine N-sulfate, D-glucose 6-sulfate, D-glucosamine, D-galactosamine, N-acetyl-D-glucosamine, N-acetyl-D-galactosamine, D-xylose, D-glucuronic acid
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