Abstract
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.
MeSH terms
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Animals
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Apoptosis
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High-Temperature Requirement A Serine Peptidase 2
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Inhibitor of Apoptosis Proteins
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Mice
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Mitochondria / enzymology
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Mitochondria / physiology*
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Mitochondrial Proteins / chemistry
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Mitochondrial Proteins / metabolism
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Neurodegenerative Diseases / enzymology*
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Neurodegenerative Diseases / genetics
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Neurodegenerative Diseases / pathology*
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Protein Binding
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Protein Denaturation
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Protein Folding
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Proteins / metabolism
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Serine Endopeptidases / metabolism*
Substances
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Inhibitor of Apoptosis Proteins
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Mitochondrial Proteins
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Proteins
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Serine Endopeptidases
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High-Temperature Requirement A Serine Peptidase 2
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Htra2 protein, mouse