EC Number   |
General Information |
Reference |
|---|
   3.4.24.71 | malfunction |
ECE-1 inhibition causes endosomal retention of the substance P neurokinin 1 receptor, beta-arrestins, and Src, resulting in markedly sustained ERK2 activation in the cytosol and nucleus, whereas ECE-1 overexpression attenuates ERK2 activation. ECE-1 inhibition also enhances substance P-induced expression and phosphorylation of the nuclear death receptor Nur77, resulting in cell death |
709039 |
| 3.4.24.71 | malfunction |
ECE-1 inhibition causes endosomal retention of the substance P neurokinin 1 receptor, beta-arrestins, and Src, resulting in markedly sustained ERK2 activation in the cytosol and nucleus. ECE-1 inhibition also enhances substance P-induced expression and phosphorylation of the nuclear death receptor Nur77, resulting in cell death |
709039 |
| 3.4.24.71 | malfunction |
enzyme inhibition increases glucagon-like peptide 1-induced activation of extracellular signal-regulated kinase and generation of cAMP. Enzyme inhibition blocks resensitisation of glucagon-like peptide 1 7-36 amide-mediated Ca2+ signalling |
752727 |
| 3.4.24.71 | malfunction |
siRNA-mediated knockdown of ECE-1 results in a significant reduction in FAK phosphorylation. Transient ECE-1 overexpression in PNT1-a cells increases FAK phosphorylation |
719207 |
| 3.4.24.71 | metabolism |
regulation of neuropeptide signaling at the cell surface involving ECE-1, detailed overview |
709039 |
| 3.4.24.71 | metabolism |
the enzyme regulates glucagon-like peptide-1 receptor signalling and resensitisation |
752727 |
| 3.4.24.71 | physiological function |
by degrading substance P and destabilizing endosomal signalosomes, ECE-1 has a dual role in controlling endocytic signalling and trafficking of the NK1R: promoting resensitization of G protein-mediated plasma membrane signalling, and terminating beta-arrestin-mediated endosomal signalling |
720315 |
| 3.4.24.71 | physiological function |
differential degradation by ECE-1 is a novel mechanism by which corticotropin-releasing factor receptor 1 is protected from overactivation by physiologically relevant high concentrations of higher affinity ligand to mediate distinct resensitization and downstream signaling |
720472 |
| 3.4.24.71 | physiological function |
ECE-1 influences PC cell invasion via both ET-1-mediated FAK phosphorylation and ET-1 independent mechanisms |
719207 |
| 3.4.24.71 | physiological function |
ECE-1 regulates the duration and subcellular location of substance P-induced, beta-arrestin-dependent ERK activation, overview |
709039 |
