Preparing your results

Our searching services are busy right now. Your search will reload in five seconds.

X
Forgot Password

If you have forgotten your password you can enter your email here and get a temporary password sent to your email.

The serine protease Omi/HtrA2 is released from mitochondria during apoptosis. Omi interacts with caspase-inhibitor XIAP and induces enhanced caspase activity.

http://www.ncbi.nlm.nih.gov/pubmed/11803371

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.

Pubmed ID: 11803371 RIS Download

Mesh terms: Amino Acid Sequence | Animals | Apoptosis | BH3 Interacting Domain Death Agonist Protein | Carrier Proteins | Caspases | Cells, Cultured | Cytosol | Enzyme Activation | Mice | Mice, Inbred C57BL | Mice, Transgenic | Mitochondria | Mitochondrial Proteins | Molecular Sequence Data | Proteins | Serine Endopeptidases | Translocation, Genetic | X-Linked Inhibitor of Apoptosis Protein