Cookies on this website

We use cookies to ensure that we give you the best experience on our website. If you click 'Accept all cookies' we'll assume that you are happy to receive all cookies and you won't see this message again. If you click 'Reject all non-essential cookies' only necessary cookies providing core functionality such as security, network management, and accessibility will be enabled. Click 'Find out more' for information on how to change your cookie settings.

Mammalian mitochondrial HtrA2/Omi was originally described as an apoptosis inducer, but rather than having extra cells, mice with mutant HtrA2/Omi suffer from a neurodegenerative disease due to progressive mitochondrial damage. This suggests that instead of promoting cell death by antagonizing inhibitor of apoptosis (IAP) proteins, the primary function of HtrA2/Omi is to handle misfolded proteins in the mitochondria.


Journal article

Publication Date





251 - 253


Animals, Apoptosis, High-Temperature Requirement A Serine Peptidase 2, Inhibitor of Apoptosis Proteins, Mice, Mitochondria, Mitochondrial Proteins, Neurodegenerative Diseases, Protein Binding, Protein Denaturation, Protein Folding, Proteins, Serine Endopeptidases