EC Number   |
Inhibitors |
Structure |
|---|
   2.3.2.8 | isoglutamine |
- |
   |
| 2.3.2.8 | L-Glu-L-Val-L-Phe |
- |
|
| 2.3.2.8 | merbromin |
- |
|
| 2.3.2.8 | more |
no inhibition by puromycin |
|
| 2.3.2.8 | more |
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 |
|
| 2.3.2.8 | more |
antibodies to hog enzyme prepared in rabbit |
|
| 2.3.2.8 | more |
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 |
|
| 2.3.2.8 | more |
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 |
|
| 2.3.2.8 | N-ethylmaleimide |
rapid inactivation at 0.2 mM |
|
| 2.3.2.8 | p-[(bromoacetyl)amino]phenylarsenoxide |
irreversible, potent inhibitor |
|
