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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.

Type

Journal article

Publication Date

31/10/2003

Volume

115

Pages

251 - 253

Keywords

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