ArticleFree radical biology & medicine2021
Oxidized GAPDH transfers S-glutathionylation to a nuclear protein Sirtuin-1 leading to apoptosis.
Article in Free radical biology & medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 44 citations in OpenAlex.
- Glutathione Biology in Neurodegenerative and Metabolic Diseases: Molecular Mechanisms, Pathophysiological Roles, and Therapeutic Perspectives.International journal of molecular sciences · 2026Review
- Subcellular localization as a driver of protein function.Nature reviews. Molecular cell biology · 2026Review
- Enhanced Therapeutic Effects of Extracellular Vesicles Targeting MiR-137 Contribute to Functional Recovery by Attenuating Neuronal Injury After Ischemic Stroke.Neuroscience bulletin · 2026Article
- Protein oxidation in crowded environments.The Biochemical journal · 2026Review
- Heme-mediated selection of encapsulatedEmerging microbes & infections · 2025Article
- Energy stress-induced PKCζ S-glutathionylation is essential for LKB1 cytoplasmic translocation and AMPK activation.Life metabolism · 2025Article
- First In Silico Study of TwoInternational journal of molecular sciences · 2025Article
- USP2 reversed cisplatin resistance through p53-mediated ferroptosis in NSCLC.BMC medical genomics · 2025Article
- Genetic code expansion reveals site-specific lactylation in living cells reshapes protein functions.Nature communications · 2025Article
- Disulfidptosis: a new target for central nervous system disease therapy.Frontiers in neuroscience · 2025Review
- RSL3 sensitizes glioma cells to ionizing radiation by suppressing TGM2-dependent DNA damage repair and epithelial-mesenchymal transition.Redox biology · 2024Article
- Characterization of naphthoquinones as inhibitors of glutathione reductase and inducers of intracellular oxidative stress.Redox report : communications in free radical research · 2024Article
- Metabolic Responses to Redox Stress in Vascular Cells.Antioxidants & redox signaling · 2024Review
- Drivers of cardiovascular disease in metabolic dysfunction-associated steatotic liver disease: the threats of oxidative stress.Frontiers in cardiovascular medicine · 2024Review
- Mechanisms Underlying the Therapeutic Effects of Nicotinamide Mononucleotide in Treating High-fat Diet-induced Hypertrophic Cardiomyopathy based on GEO Datasets, Network Pharmacology, and Molecular Docking.Current pharmaceutical design · 2024Article
- Identification of biomarkers and potential drug targets in osteoarthritis based on bioinformatics analysis and mendelian randomization.Frontiers in pharmacology · 2024Article
- Review
- Sirtuins at the Crossroads between Mitochondrial Quality Control and Neurodegenerative Diseases: Structure, Regulation, Modifications, and Modulators.Aging and disease · 2023Review
- Origin of Elevated S-Glutathionylated GAPDH in Chronic Neurodegenerative Diseases.International journal of molecular sciences · 2023Article
- GAPDH: unveiling its impact as a key hypoxia-related player in head and neck squamous cell carcinoma tumor progression, prognosis, and therapeutic potential.American journal of cancer research · 2023Article
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
aimsS-glutathionylation is a reversible oxidative modification of protein cysteines that plays a critical role in redox signaling. Glutaredoxin-1 (Glrx), a glutathione-specific thioltransferase, removes protein S-glutathionylation. Glrx, though a cytosolic protein, can activate a nuclear protein Sirtuin-1 (SirT1) by removing its S-glutathionylation. Glrx ablation causes metabolic abnormalities and promotes controlled cell death and fibrosis in mice. Glyceraldehyde 3-phosphate dehydrogenase (GAPDH), a key enzyme of glycolysis, is sensitive to oxidative modifications and involved in apoptotic signaling via the SirT1/p53 pathway in the nucleus. We aimed to elucidate the extent to which S-glutathionylation of GAPDH and glutaredoxin-1 contribute to GAPDH/SirT1/p53 apoptosis pathway.
resultsExposure of HEK 293T cells to hydrogen peroxide (H
conclusionsAbundant GAPDH with its highly reactive-cysteine thiolate may function as a cytoplasmic rheostat to sense oxidative stress. S-glutathionylation of GAPDH may relay the signal to the nucleus where GAPDH trans-glutathionylates nuclear proteins such as SirT1 to initiate apoptosis. Glrx reverses GAPDH S-glutathionylation and prevents its nuclear translocation and cytoplasmic-nuclear redox signaling leading to apoptosis. Our data suggest that trans-glutathionylation is a critical step in apoptotic signaling and a potential mechanism that cytosolic Glrx controls nuclear transcription factors.
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