EC Number   |
General Information |
Reference |
|---|
   3.4.21.108 | physiological function |
silencing endogenous expression of HtrA2/Omi with siRNA results in aggregated endoplasmic reticulum stress and cell death. The expression level of HtrA2/Omi decreases with endoplasmic reticulum stress induction in 6-hydroxydopamine-treated SH-SY5Y cells |
732357 |
| 3.4.21.108 | physiological function |
the enzyme is involved in the cytoskeletal reorganization that accompanies radiation-induced senescence and the continuous maintenance of proliferation arrest |
774369 |
| 3.4.21.108 | physiological function |
the enzyme plays a crucial role in apoptosis by cleaving inhibitory and anti-apoptotic proteins by translocating from mitochondria to the cytosol |
768982 |
| 3.4.21.108 | physiological function |
the enzyme plays a dual role in maintenance of parasite mitochondria under normal conditions, as well as regulation of programmed cell death under cellular stress conditions. The enzyme activity is not essential for parasite survival |
775403 |
| 3.4.21.108 | physiological function |
the enzyme plays an essential role in regulating the adipogenesis-associated hair cycle |
769073 |
| 3.4.21.108 | physiological function |
the HtrA2-mediated Parkin cleavage irreversibly disrupts Parkin-mediated synphilin-1 ubiquitination and autoubiquitination, indicating that HtrA2 may play a critical role in the Parkin-related pathway involved in the ubiquitin proteasome system |
707374 |
| 3.4.21.108 | physiological function |
The inhibition of HtrA2 by specific inhibitor UCF-101 or by shRNA reduces lipopolysaccharide-induced brain endothelial cell apoptosis, and results in significant improvement on lipopolysaccharide-induced blood-brain-barrier disruption as well as decreased occludin, claudin-5 and ZO-1 expressions. HtrA2 manipulates endothelial cell apoptosis by shifting into cytosol and inducing X-linked inhibitor of apoptosis protein (XIAP) degradation. UCF-101 administration or HtrA2 shRNA intervention attenuates the degradation of XIAP, poly-ADP-ribose polymerase (PARP), cleavage, and caspase-3 cleavage. UCF-101 partly prevents the mobilization of HtrA2 from the mitochondria to the cytosol after lipopolysaccharide intervention |
753695 |
| 3.4.21.108 | physiological function |
the PDZ domain is dispensable for HtrA3 activity |
755093 |
