Literature summary for 3.4.21.108 extracted from

Hu, Y.; Bi, Y.; Yao, D.; Wang, P.; Li, Y.
Omi/HtrA2 protease associated cell apoptosis participates in blood-brain barrier dysfunction (2019), Front. Mol. Neurosci., 12, 48 .

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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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Release 2023.1 (January 2023)