EC Number   |
General Information |
Reference |
|---|
   3.4.21.108 | malfunction |
decreased enzyme function damages mitochondrial quality in the heterozygous mouse brain cortex, leading to more brain ischemia/reperfusion injury. HtrA2-heterozygous mice show decreased mitochondrial quality control and reduced mitochondrial function after ischemia/reperfusion injury, decreased anti-damage ability and increased apoptosis after middle cerebral artery occlusion |
771822 |
| 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 | malfunction |
enzyme inactivation leads to the growth retardation of adipocytes, thereby delaying the hair cycle of mnd2 mice |
769073 |
| 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 | malfunction |
in mouse embryonic HtrA2/omi knockout fibroblast cells the apoptosis-dependent cleavage of Wilms'tumor suppressor protein WT1 is prevented and expression of WT1 is upregulated |
709955 |
| 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 |
knockdown of HtrA2/Omi affords protection against interleukin-3 withdrawal-induced death in the presence of carbobenzoxy-valyl-analylaspartyl-[O-methyl]-fluoromethylketone |
717463 |
| 3.4.21.108 | malfunction |
knockdown of Omi decreases the basal level of autophagy and increases the level of neurodegenerative proteins such as pathogenic A53T alpha-synuclein and truncated polyglutamine-expanded huntingtin, as well as the endogenous autophagy substrate p62 |
711699 |
