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Mitochondrial defects and neurodegeneration in mice overexpressing wild-type or G399S mutant HtrA2.

Human molecular genetics - 1 Feb 2016

Casadei Nicolas, Sood Poonam, Ulrich Thomas, Fallier-Becker Petra, Kieper Nicole, Helling Stefan, May Caroline, Glaab Enrico, Chen Jing, Nuber Silke, Wolburg Hartwig, Marcus Katrin, Rapaport Doron, Ott Thomas, Riess Olaf, Krüger Rejko, Fitzgerald Julia C

Abstract excerpt

The protease HtrA2 has a protective role inside mitochondria, but promotes apoptosis under stress. We previously identified the G399S HtrA2 mutation in Parkinson's disease (PD) patients and reported mitochondrial dysfunction in vitro. Mitochondrial dysfunction is a common feature of PD and related to neurodegeneration. Complete loss of HtrA2 has been shown to cause neurodegeneration in mice. However, the full...

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PMID: 26604148
DOI: 10.1093/hmg/ddv485

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PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 5 Sept 2026. Manifest publication-graph-cohort-2026-09-05.1.

Source receipt: pubmed, retrieved 5 Sept 2026.

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Mitochondrial defects and neurodegeneration in mice overexpressing wild-type or G399S mutant HtrA2.PMID 26604148Read ↗

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