ArticleThe Journal of biological chemistry2015
Functional significance of point mutations in stress chaperone mortalin and their relevance to Parkinson disease.
Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
24 citing papers in PubMed, 44 citations in OpenAlex.
- Review
- Autophagy inhibition rescues structural and functional defects caused by the loss of mitochondrial chaperoneAutophagy · 2021Article
- RNA-seq profiling reveals PBMC RNA as a potential biomarker for hepatocellular carcinoma.Scientific reports · 2021Article
- The mitochondrial PKCδ/retinol signal complex exerts real-time control on energy homeostasis.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2020Review
- Novel Caffeic Acid Phenethyl Ester-Mortalin Antibody Nanoparticles Offer Enhanced Selective Cytotoxicity to Cancer Cells.Cancers · 2020Article
- Overexpression of PGC-1α influences the mitochondrial unfolded protein response (mtUPR) induced by MPPScientific reports · 2020Article
- Effect of fosinopril on the renal cortex protein expression profile of Otsuka Long-Evans Tokushima Fatty rats.Experimental and therapeutic medicine · 2020Article
- Oxidative Stress in Parkinson's Disease: Potential Benefits of Antioxidant Supplementation.Oxidative medicine and cellular longevity · 2020Review
- Marine Carotenoid Fucoxanthin Possesses Anti-Metastasis Activity: Molecular Evidence.Marine drugs · 2019Article
- Biophysical Consequences of EVEN-PLUS Syndrome Mutations for the Function of Mortalin.The journal of physical chemistry. B · 2019Article
- Oxidation resistance 1 regulates post-translational modifications of peroxiredoxin 2 in the cerebellum.Free radical biology & medicine · 2019Article
- Molecular mechanisms of proteinopathies across neurodegenerative disease: a review.Neurological research and practice · 2019Review
- Mortalin stabilizes CD151-depedent tetraspanin-enriched microdomains and implicates in the progression of hepatocellular carcinoma.Journal of Cancer · 2019Article
- Lifelong Football Training: Effects on Autophagy and Healthy Longevity Promotion.Frontiers in physiology · 2019Article
- The genetic architecture of mitochondrial dysfunction in Parkinson's disease.Cell and tissue research · 2018Review
- Multi-chaperone function modulation and association with cytoskeletal proteins are key features of the function of AIP in the pituitary gland.Oncotarget · 2018Article
- Essential Roles of E3 Ubiquitin Ligases in p53 Regulation.International journal of molecular sciences · 2017Review
- Relevance of mortalin to cancer cell stemness and cancer therapy.Scientific reports · 2017Article
- Protein misfolding in neurodegenerative diseases: implications and strategies.Translational neurodegeneration · 2017Review
- Chaperone-Based Therapies for Disease Modification in Parkinson's Disease.Parkinson's disease · 2017Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mortalin/mtHsp70/Grp75 (mot-2), a heat shock protein 70 family member, is an essential chaperone, enriched in cancers, and has been shown to possess pro-proliferative and anti-apoptosis functions. An allelic form of mouse mortalin (mot-1) that differs by two amino acids, M618V and G624R, in the C terminus substrate-binding domain has been reported. Furthermore, genome sequencing of mortalin from Parkinson disease patients identified two missense mutants, R126W and P509S. In the present study, we investigated the significance of these mutations in survival, proliferation, and oxidative stress tolerance in human cells. Using mot-1 and mot-2 recombinant proteins and specific antibodies, we performed screening to find their binding proteins and then identified ribosomal protein L-7 (RPL-7) and elongation factor-1 α (EF-1α), which differentially bind to mot-1 and mot-2, respectively. We demonstrate that mot-1, R126W, or P509S mutant (i) lacks mot-2 functions involved in carcinogenesis, such as p53 inactivation and hTERT/hnRNP-K (heterogeneous nuclear ribonucleoprotein K) activation; (ii) causes increased level of endogenous oxidative stress; (iii) results in decreased tolerance of cells to exogenous oxidative stress; and (iv) shows differential binding and impact on the RPL-7 and EF-1α proteins. These factors may mediate the transformation of longevity/pro-proliferative function of mot-2 to the premature aging/anti-proliferative effect of mutants, and hence may have significance in cellular aging, Parkinson disease pathology, and prognosis.
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