ArticleFrontiers in cellular neuroscience2015
The deafness gene DFNA5 induces programmed cell death through mitochondria and MAPK-related pathways.
Article in Frontiers in cellular neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed.
- Juvenile dermatomyositis: new insights into pathogenesis and clinical applications.Pediatric rheumatology online journal · 2025Review
- Lipin3 deficiency aggravates cisplatin induced acute kidney injury via activating Sirt1-p21-Caspase 3-GSDME pyroptosis pathway.International journal of biological sciences · 2025Article
- Gain-of-function variants in GSDME cause pyroptosis and apoptosis associated with post-lingual hearing loss.Human genetics · 2024Article
- DNA methylation patterns in the frontal lobe white matter of multiple system atrophy, Parkinson's disease, and progressive supranuclear palsy: a cross-comparative investigation.Acta neuropathologica · 2024Article
- Caspase-1 activates gasdermin A in non-mammals.eLife · 2024Article
- Distinct GSDMB protein isoforms and protease cleavage processes differentially control pyroptotic cell death and mitochondrial damage in cancer cells.Cell death and differentiation · 2023Article
- Neuronal glutathione loss leads to neurodegeneration involving gasdermin activation.Scientific reports · 2023Article
- Precise Orchestration of Gasdermins' Pore-Forming Function by Posttranslational Modifications in Health and Disease.International journal of biological sciences · 2023Review
- Role of gasdermin family proteins in the occurrence and progression of hepatocellular carcinoma.Heliyon · 2022Review
- Does Pyroptosis Play a Role in Inflammasome-Related Disorders?International journal of molecular sciences · 2022Review
- Blocking GSDME-mediated pyroptosis in renal tubular epithelial cells alleviates disease activity in lupus mice.Cell death discovery · 2022Article
- Blocking GSDME-mediated pyroptosis in renal tubular epithelial cells alleviates disease activity in lupus mice.Cell death discovery · 2022Article
- Molecular mechanisms of neuronal death in brain injury after subarachnoid hemorrhage.Frontiers in cellular neuroscience · 2022Review
- GSDME Increases Chemotherapeutic Drug Sensitivity by Inducing Pyroptosis in Retinoblastoma Cells.Oxidative medicine and cellular longevity · 2022Article
- Gasdermin E: A Prospective Target for Therapy of Diseases.Frontiers in pharmacology · 2022Review
- Mutation analysis of the GSDME gene in a Chinese family with non-syndromic hearing loss.PloS one · 2022Article
- GSDMD-mediated pyroptosis: a critical mechanism of diabetic nephropathy.Expert reviews in molecular medicine · 2021Review
- SOD2 Alleviates Hearing Loss Induced by Noise and Kanamycin in Mitochondrial DNA4834-deficient Rats by Regulating PI3K/MAPK Signaling.Current medical science · 2021Article
- Gasdermin E-mediated programmed cell death: An unpaved path to tumor suppression.Journal of Cancer · 2021Review
- Programmed cell death pathways in hearing loss: A review of apoptosis, autophagy and programmed necrosis.Cell proliferation · 2020Review
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5 authors.
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Abstract
Cell death exists in many different forms. Some are accidental, but most of them have some kind of regulation and are called programmed cell death. Programmed cell death (PCD) is a very diverse and complex mechanism and must be tightly regulated. This study investigated PCD induced by DFNA5, a gene responsible for autosomal dominant hearing loss (HL) and a tumor suppressor gene (TSG) involved in frequent forms of cancer. Mutations in DFNA5 lead to exon 8 skipping and result in HL in several families. Expression of mutant DFNA5, a cDNA construct where exon 8 is deleted, was linked to PCD both in human cell lines and in Saccharomyces cerevisiae. To further investigate the cell death mechanism induced by mutant DFNA5, we performed a microarray study in both models. We used wild-type DFNA5, which does not induce cell death, as a reference. Our data showed that the yeast pathways related to mitochondrial ATP-coupled electron transport chain, oxidative phosphorylation and energy metabolism were up-regulated, while in human cell lines, MAP kinase-related activity was up-regulated. Inhibition of this pathway was able to partially attenuate the resulting cell death induced by mutant DFNA5 in human cell lines. In yeast, the association with mitochondria was demonstrated by up-regulation of several cytochrome c oxidase (COX) genes involved in the cellular oxidative stress production. Both models show a down-regulation of protein sorting- and folding-related mechanisms suggesting an additional role for the endoplasmic reticulum (ER). The exact relationship between ER and mitochondria in DFNA5-induced cell death remains unknown at this moment, but these results suggest a potential link between the two.
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