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Literature summary for 3.4.21.108 extracted from

  • Vande Walle, L.; Wirawan, E.; Lamkanfi, M.; Festjens, N.; Verspurten, J.; Saelens, X.; Vanden Berghe, T.; Vandenabeele, P.
    The mitochondrial serine protease HtrA2/Omi cleaves RIP1 during apoptosis of Ba/F3 cells induced by growth factor withdrawal (2010), Cell Res., 20, 421-433.
    View publication on PubMed
Search for more literature for 3.4.21.108

Protein Variants

Protein Variants Comment Organism
S306A catalytically inactive mutant Mus musculus

Localization

Localization Comment Organism GeneOntology No. Textmining
cytosol
-
 Mus musculus 5829
-

Organism

Organism UniProt Comment Textmining
Mus musculus
-
-
-

Source Tissue

Source Tissue Comment Organism Textmining
BA/F3 cell
-
 Mus musculus
-

Substrates and Products (Substrate)

Substrates Comment Substrates Organism Products Comment (Products) Rev. Reac.
receptor-interacting protein 1 + H2O the HtrA2/Omi cleavage site receptor-interacting protein 1 is mapped to the intermediate domain and the corresponding N- and C-terminal fragments are impaired in their ability to activate nuclear factor-kappaB, c-Jun N-terminal kinase and p38 mitogen-activated protein kinase Mus musculus ?
-
 ?

Synonyms

Synonyms Comment Organism
high temperature requirement protein A2
-
 Mus musculus
HtrA2/Omi
-
 Mus musculus

General Information

General Information Comment Organism
malfunction knockdown of HtrA2/Omi affords protection against interleukin-3 withdrawal-induced death in the presence of carbobenzoxy-valyl-analylaspartyl-[O-methyl]-fluoromethylketone Mus musculus
physiological function HtrA2/Omi plays a role in caspase-independent cell death during growth factor withdrawal by cleaving receptor-interacting protein 1 Mus musculus