ArticleNeuroscience bulletin2017
Familial Parkinson's Disease-Associated L166P Mutant DJ-1 is Cleaved by Mitochondrial Serine Protease Omi/HtrA2.
Article in Neuroscience bulletin, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 14 citations in OpenAlex.
- Mitochondria-Associated MicroRNAs: Emerging Roles in the Pathogenesis of Parkinson's Disease.Biomedicines · 2026Review
- A Perspective on the Role of Mitochondrial Biomolecular Condensates (mtBCs) in Neurodegenerative Diseases and Evolutionary Links to Bacterial BCs.International journal of molecular sciences · 2025Review
- Review
- Light-induced primary amines and o-nitrobenzyl alcohols cyclization as a versatile photoclick reaction for modular conjugation.Nature communications · 2020Article
- Prodromal Markers of Parkinson's Disease in Patients With Essential Tremor.Frontiers in neurology · 2020Review
- Poly-PR in C9ORF72-Related Amyotrophic Lateral Sclerosis/Frontotemporal Dementia Causes Neurotoxicity by Clathrin-Dependent Endocytosis.Neuroscience bulletin · 2019Article
- Disease-Associated Genetic Variation in Human Mitochondrial Protein Import.American journal of human genetics · 2019Review
- Pharmacological activation of REV-ERBα represses LPS-induced microglial activation through the NF-κB pathway.Acta pharmacologica Sinica · 2019Article
- The Role of the Antioxidant Response in Mitochondrial Dysfunction in Degenerative Diseases: Cross-Talk between Antioxidant Defense, Autophagy, and Apoptosis.Oxidative medicine and cellular longevity · 2019Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Parkinson's disease (PD) is the most common neurodegenerative movement disorder. Mutations in the DJ-1, including L166P, are responsible for recessive early-onset PD. Many lines of evidence have shown that L166P is not only a loss-of-function mutant, but also a pro-apoptotic-like protein that results in mitochondrial dysfunction. L166P has been reported to be unstable and to mislocalize to mitochondria. However, the mechanisms underlying the instability of L166P compared to wild-type DJ-1 remain largely unknown. Here, we showed that Omi/HtrA2, a mitochondrial serine protease that has also been linked to the pathogenesis of PD, contributed to L166P instability. Omi directly interacted with and cleaved L166P in mitochondria to decrease the L166P level. However, Omi did not bind and cleave wild-type DJ-1. Moreover, Omi cleaved L166P at both serine residues 3 and 121, while L166P-induced cell death under H
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.