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Literature summary extracted from

  • Liu, Q.B.; Liu, L.L.; Lu, Y.M.; Tao, R.R.; Huang, J.Y.; Shioda, N.; Moriguchi, S.; Fukunaga, K.; Han, F.; Lou, Y.J.
    The induction of reactive oxygen species and loss of mitochondrial Omi/HtrA2 is associated with S-nitrosoglutathione-induced apoptosis in human endothelial cells (2010), Toxicol. Appl. Pharmacol., 244, 374-384.
    View publication on PubMed

Localization

EC Number Localization Comment Organism GeneOntology No. Textmining
3.4.21.108 cytoplasm Omi/HtrA2 is principally localized to the cytoplasm Homo sapiens 5737
-
3.4.21.108 mitochondrion S-nitrosoglutathione treatment induces redistribution of Omi/HtrA2 from cytoplasm to mitochondria in endothelial cells Homo sapiens 5739
-

Organism

EC Number Organism UniProt Comment Textmining
3.4.21.108 Homo sapiens
-
-
-

Source Tissue

EC Number Source Tissue Comment Organism Textmining
3.4.21.108 EAhy 926 cell
-
 Homo sapiens
-
3.4.21.108 endothelial cell
-
 Homo sapiens
-

Synonyms

EC Number Synonyms Comment Organism
3.4.21.108 Omi/HtrA2
-
 Homo sapiens

Expression

EC Number Organism Comment Expression
3.4.21.108 Homo sapiens S-nitrosoglutathione treatment significantly decreases mitochondrial Omi/HtrA2 content after 8 h of exposure in endothelial cells down
3.4.21.108 Homo sapiens S-nitrosoglutathione treatment significantly increases cytosolic Omi/HtrA2 content after 8 h of exposure in endothelial cells up

General Information

EC Number General Information Comment Organism
3.4.21.108 malfunction loss of mitochondrial Omi/HtrA2 is associated with S-nitrosoglutathione-induced apoptosis in human endothelial cells Homo sapiens