HtrA2/Omi, a sheep in wolf's clothing.
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.
Vaux
David L
DL
The Walter and Eliza Hall Institute, 1G Royal Parade, Parkville, 3050, Victoria, Australia
Silke
John
J
D000818:Animals; D017209:Apoptosis; D000074923:High-Temperature Requirement A Serine Peptidase 2; D051034:Inhibitor of Apoptosis Proteins; D051379:Mice; D008928:Mitochondria / Q000201:enzymology / Q000502:physiology*; D024101:Mitochondrial Proteins / Q000737:chemistry / Q000378:metabolism; D019636:Neurodegenerative Diseases / Q000201:enzymology* / Q000235:genetics / Q000473:pathology*; D011485:Protein Binding; D011489:Protein Denaturation; D017510:Protein Folding; D011506:Proteins / Q000378:metabolism; D012697:Serine Endopeptidases / Q000378:metabolism*
D051034:Inhibitor of Apoptosis Proteins; D024101:Mitochondrial Proteins; D011506:Proteins; D012697:Serine Endopeptidases; D000074923:High-Temperature Requirement A Serine Peptidase 2; C000615915:Htra2 protein, mouse