EC Number   |
General Information |
Reference  |
|---|
   3.4.21.108 | physiological function |
Omi/HtrA2 interacts with thanatos-associated protein 5 in mammalian cells during apoptosis |
707066 |
| 3.4.21.108 | malfunction |
endogenous levels of Parkin are significantly decreased in wild-type (HtrA2+/+) mouse embryonic fibroblasts compared with those in HtrA2-knockout (HtrA2-/-) mouse embryonic fibroblasts under the same stress conditions |
707374 |
| 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 | malfunction |
in Omi/HtrA2 knockout mouse embryonic fibroblasts elongated mitochondria are found by live cell imaging. Electron microscopy confirm the mitochondrial morphology alterations and show abnormal cristae structure. Examining the levels of proteins involved in mitochondrial fusion, a selective up-regulation of optic atrophy protein 1 is shown. Complementation of knockout cells with human wild-type Omi/HtrA2 reverses the mitochondrial elongation phenotype and optic atrophy protein 1 alterations |
708415 |
| 3.4.21.108 | malfunction |
in Omi/HtrA2 silenced Drosophila S2R+ cells elongated mitochondria are found by live cell imaging. Electron microscopy confirm the mitochondrial morphology alterations and show abnormal cristae structure. Examining the levels of proteins involved in mitochondrial fusion, a selective up-regulation of optic atrophy protein 1 is shown |
708415 |
| 3.4.21.108 | malfunction |
in Omi/HtrA2 silenced human HeLa elongated mitochondria are found by live cell imaging. Electron microscopy confirm the mitochondrial morphology alterations and show abnormal cristae structure. Examining the levels of proteins involved in mitochondrial fusion, a selective up-regulation of optic atrophy protein 1 is shown |
708415 |
| 3.4.21.108 | malfunction |
Omi/HtrA2 knockout mice show significant increase in intramitochondrial reactive oxygen species and decreased mitochondrial membrane potential in MEF cells |
708415 |
| 3.4.21.108 | physiological function |
Omi/HtrA2 functionally and physically interacts with the mitochondrial fusion protein OPA1. Mitochondrial morphology relies on Omi/HtrA2 protease function |
708415 |
| 3.4.21.108 | malfunction |
fewer and abnormal mitochondria are found in HtrA2/Omi knockout mice photoreceptors and pigment epithelial cells |
708821 |
| 3.4.21.108 | physiological function |
HtrA2 has a moderate ability to delay the aggregation of citrate synthase in vitro. Additionally, using electron microscopy and nuclear magnetic resonance analyses, it is observed that HtrA2 significantly delays the aggregation of the Abeta1-42 peptide. The protease activity of HtrA2 and its PDZ domain are not essential for the delay of Abeta1-42 peptide aggregation |
708862 |
