The serine protease Omi/HtrA2 is released from mitochondria during apoptosis. Omi interacts with caspase-inhibitor XIAP and induces enhanced caspase activity.
Cell Death Differ
; 9(1): 20-6, 2002 Jan.
Article
em En
| MEDLINE
| ID: mdl-11803371
ABSTRACT
Proteome analysis of supernatant of isolated mitochondria exposed to recombinant tBid, a proapoptotic Bcl-2 member, revealed the presence of the serine protease Omi, also called HtrA2. This release was prevented in mitochondria derived from Bcl-2-transgenic mice. Release of Omi under apoptotic conditions was confirmed in vivo in livers from mice injected with agonistic anti-Fas antibodies and was prevented in livers from Bcl-2 transgenic mice. Omi release also occurs in apoptotic dying but not in necrotic dying fibrosarcoma L929 cells, treated with anti-Fas antibodies and TNF, respectively. The amino acid sequence reveals the presence of an XIAP interaction motif at the N-terminus of mature Omi. We demonstrate an interaction between endogeneous Omi and recombinant XIAP. Furthermore we show that endogenous Omi is involved in enhanced activation of caspases in cytosolic extracts.
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Base de dados:
MEDLINE
Assunto principal:
Serina Endopeptidases
/
Proteínas
/
Apoptose
/
Caspases
/
Mitocôndrias
Limite:
Animals
Idioma:
En
Ano de publicação:
2002
Tipo de documento:
Article