ArticleThe Biochemical journal2012
Mitochondrial c-Src regulates cell survival through phosphorylation of respiratory chain components.
Article in The Biochemical journal, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers, 1 of them a synthesis that pooled it.
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Who cites it
51 citing papers in PubMed, 1 synthesis or guideline pooled it, 99 citations in OpenAlex.
- The Association Between Serum Gamma-Glutamyl Transferase and Gastrointestinal Cancer Risk: A Systematic Review and Meta-Analysis.Cancer medicine · 2025Pooled it
- N-Myristoyltransferase 2 Is Regulated by Polyphosphate-Driven Lysine Interactions.Biomolecules · 2026Article
- SBK2 Links Cardiac Stress Signaling to Mitochondrial Proteostasis.Circulation research · 2026Article
- MYC_V1-Related Genes Affect Gastric Cancer Proliferation by Regulating Energy Metabolism and Analysis of Therapeutic Targets.International journal of molecular sciences · 2026Article
- CDCP1/mitochondrial Src axis increases electron transport chain function to promote metastasis in triple-negative breast cancer.British journal of cancer · 2025Article
- Cardiac TRPM7 Causes Diabetic Heart Failure With Preserved Ejection Fraction.JACC. Basic to translational science · 2025Article
- SDH defective cancers: molecular mechanisms and treatment strategies.Cell biology and toxicology · 2025Review
- Restoration of pp60International journal of molecular sciences · 2025Article
- Parkinson's disease and glucose metabolism impairment.Translational neurodegeneration · 2025Review
- Serine phosphorylation facilitates protein degradation by the human mitochondrial ClpXP protease.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- A multiplex method for rapidly identifying viral protease inhibitors.Molecular systems biology · 2025Article
- c-Src Is Responsible for Mitochondria-Mediated Arrhythmic Risk in Ischemic Cardiomyopathy.Circulation. Arrhythmia and electrophysiology · 2024Article
- Comprehensive overview of how to fade into succinate dehydrogenase dysregulation in cancer cells by naringenin-loaded chitosan nanoparticles.Genes & nutrition · 2024Review
- Mitochondrial P-JNK target, SAB (SH3BP5), in regulation of cell death.Frontiers in cell and developmental biology · 2024Review
- Uncovering the Early Events Associated with Oligomeric Aβ-Induced Src Activation.Antioxidants (Basel, Switzerland) · 2023Article
- The roles of molecular chaperones in regulating cell metabolism.FEBS letters · 2023Review
- Orchestration of Mitochondrial Function and Remodeling by Post-Translational Modifications Provide Insight into Mechanisms of Viral Infection.Biomolecules · 2023Review
- Mechanisms of mitochondrial respiratory adaptation.Nature reviews. Molecular cell biology · 2022Review
- Src: coordinating metabolism in cancer.Oncogene · 2022Review
- Association between single-nucleotide polymorphism rs145497186 related to NDUFV2 and lumbar disc degeneration: a pilot case-control study.Journal of orthopaedic surgery and research · 2022Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondrial protein tyrosine phosphorylation is an important mechanism for the modulation of mitochondrial functions. In the present study, we have identified novel substrates of c-Src in mitochondria and investigated their function in the regulation of oxidative phosphorylation. The Src family kinase inhibitor PP2 {amino-5-(4-chlorophenyl)-7-(t-butyl) pyrazolo [3,4d] pyrimidine} exhibits significant reduction of respiration. Similar results were obtained from cells expressing kinase-dead c-Src, which harbours a mitochondrial-targeting sequence. Phosphorylation-site analysis selects c-Src targets, including NDUFV2 (NADH dehydrogenase [ubiquinone] flavoprotein 2) at Tyr(193) of respiratory complex I and SDHA (succinate dehydrogenase A) at Tyr(215) of complex II. The phosphorylation of these sites by c-Src is supported by an in vivo assay using cells expressing their phosphorylation-defective mutants. Comparison of cells expressing wild-type proteins and their mutants reveals that NDUFV2 phosphorylation is required for NADH dehydrogenase activity, affecting respiration activity and cellular ATP content. SDHA phosphorylation shows no effect on enzyme activity, but perturbed electron transfer, which induces reactive oxygen species. Loss of viability is observed in T98G cells and the primary neurons expressing these mutants. These results suggest that mitochondrial c-Src regulates the oxidative phosphorylation system by phosphorylating respiratory components and that c-Src activity is essential for cell viability.
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