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Article

Loss-of-function analysis suggests that Omi/HtrA2 is not an essential component of the PINK1/PARKIN pathway in vivo.

The Journal of neuroscience : the official journal of the Society for Neuroscience - 31 Dec 2008

Yun Jina, Cao Joseph H, Dodson Mark W, Clark Ira E, Kapahi Pankaj, Chowdhury Ruhena B, Guo Ming

Abstract excerpt

Recently, a mutation in the mitochondrial protease Omi/HtrA2, G399S, was found in sporadic Parkinson's disease (PD) patients, leading to the designation of Omi/HtrA2 as PD locus 13 (PARK13). G399S reportedly results in reduced Omi protease activity. In vitro studies have suggested that Omi/HtrA2 acts downstream of PINK1, mutations in which mediate recessive forms of PD. We, as well as other, have previously shown...

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Identifiers

PMID: 19118185
DOI: 10.1523/JNEUROSCI.5141-08.2008
PMCID: PMC2718055

Genes

PINK1

Variants

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

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Research trail→

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Loss-of-function analysis suggests that Omi/HtrA2 is not an essential component of the PINK1/PARKIN pathway in vivo.PMID 19118185Read ↗

Loss of function mutations in the gene encoding Omi/HtrA2 in Parkinson's diseaseSemantic proximity Read ↗

Drosophila HtrA2 is dispensable for apoptosis but acts downstream of PINK1 independently from Parkin.Semantic proximity Read ↗

Rhomboid-7 and HtrA2/Omi act in a common pathway with the Parkinson’s disease factors Pink1 and ParkinSemantic proximity Read ↗

Mitochondrial defects and neurodegeneration in mice overexpressing wild-type or G399S mutant HtrA2.Semantic proximity Read ↗

Genetic variation of Omi/HtrA2 and Parkinson's disease.Semantic proximity Read ↗

Parkin is not required to sustain OXPHOS function in adult mammalian tissuesSemantic proximity Read ↗

PARKIN is not required to sustain OXPHOS function in adult mammalian tissuesSemantic proximity Read ↗

The mitochondrial protease HtrA2 is regulated by Parkinson's disease-associated kinase PINK1.Semantic proximity Read ↗

Loss of HtrA2/Omi activity in non-neuronal tissues of adult mice causes premature aging.Semantic proximity Read ↗

Mortalin mutations are not a frequent cause of early-onset Parkinson disease.Semantic proximity Read ↗

Neuroprotective role of the Reaper-related serine protease HtrA2/Omi revealed by targeted deletion in mice.Semantic proximity Read ↗

HtrA2/Omi deficiency causes damage and mutation of mitochondrial DNA.Semantic proximity Read ↗

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