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Literature summary for 3.4.21.108 extracted from
- Omi/HtrA2 protease associated cell apoptosis participates in blood-brain barrier dysfunction (2019), Front. Mol. Neurosci., 12, 48 .
Localization
| Localization | Comment | Organism | GeneOntology No. | Textmining |
|---|---|---|---|---|
| mitochondrion | - |
Homo sapiens | 5739 | - |
Organism
| Organism | UniProt | Comment | Textmining |
|---|---|---|---|
| Homo sapiens | O43464 | - |
- |
Source Tissue
| Source Tissue | Comment | Organism | Textmining |
|---|---|---|---|
| HCMEC/D3 cell | - |
Homo sapiens | - |
Synonyms
| Synonyms | Comment | Organism |
|---|---|---|
| Omi/HtrA2 | - |
Homo sapiens |
General Information
| General Information | Comment | Organism |
|---|---|---|
| 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 | Homo sapiens |
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