ArticleCell death and differentiation2025
TRIM21-driven K63-linked ubiquitination of RBM38c, as a novel interactor of BECN1, contributes to DNA damage-induced autophagy.
Article in Cell death and differentiation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed.
- Article
- Unraveling the Multifaceted Role of TRIM21 in Virus-Triggered Innate Immunity and Diseases.Biomolecules · 2026Review
- XPO1-mediated TRIM21 nuclear export reprograms TREM2+ macrophage polarization by targeting IRF3 to augment anti-PD-1 efficacy in small cell lung cancer.Nature communications · 2026Article
- USP22 suppresses trophoblast cell necroptosis in preeclampsia by stabilizing KAT2A-mediated histone acetylation at the SFRP1 promoter.Journal of translational medicine · 2026Article
- SPSB3-mediated K48- and K63- linked ubiquitination and degradation of TUFM promote apoptosis induced by myocardial ischemia/reperfusion injury.Cell biology and toxicology · 2026Article
- Role of PTK6 in the diagnosis, prognosis, and immune infiltration of pancreatic cancer based on evidence from bioinformatics analysis and experimental validation.Discover oncology · 2026Article
- The ATG14: multi-layer autophagy control and an emerging therapeutic target in cancer.Apoptosis : an international journal on programmed cell death · 2026Review
- Senescence-associated secretory phenotype: the "pathogenic" factor driving orthopedic degenerative diseases and its regulation.Frontiers in aging · 2026Review
- LncRNA HYMAI Promotes Endothelial Cell Autophagy via miR-19a-3p/ ATG14 to Attenuate the Progression of Coronary Atherosclerotic Disease.Current medicinal chemistry · 2026Article
- Dual targeting of the UPS and autophagy as a novel therapy for neurodegenerative proteinopathies.Frontiers in cellular neuroscience · 2026Review
- Unraveling autophagy-metabolism crosstalk in cancer: Molecular insights and therapeutic strategies.Theranostics · 2026Review
- The role of TRIM proteins in the pathogenesis of mycobacterium tuberculosis.Biology direct · 2025Review
- OTUB1 antagonizes TRIM21 to induce deubiquitination of SPHK1 and promote the progression of hepatocellular carcinoma.Oncogene · 2025Article
- Cellular senescence in cancer: from mechanism paradoxes to precision therapeutics.Molecular cancer · 2025Review
- Evolutionary Conservation and Functional Diversification of the Rbm24/38 Family in Metazoans.Wiley interdisciplinary reviews. RNAReview
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Authors and funding
9 authors.
Funding
Abstract
Autophagy is essential in DNA damage response by limiting damage, but its responsive activation remains unclear. RBM38 (RBM38a), an RNA-binding protein, regulates mRNA metabolism and plays a key role in controlling cell cycle progression, senescence, and cancer. In this study, we uncovered a novel primate-specific isoform, RBM38c, with 32 extra amino acids from exon 2, which imparts a distinct capacity to promote autophagy upon DNA damage. TP53 increases RBM38c expression upon DNA damage, while TRIM21 facilitates its K63-linked ubiquitination at lysine (K) 35. Activated RBM38c enhances its interaction with BECN1, promoting the formation of the ATG14-containing PtdIns3K-C1 complex and thus autophagy initiation. A K35R mutation or TRIM21 deficiency impairs RBM38c ubiquitination, preventing autophagy activation upon DNA damage. Moreover, RBM38c-driven autophagy protects cells from DNA damage-induced apoptosis and promotes survival, with this beneficial effect susceptible to suppression by the autophagy inhibitor 3-methyladenine. Consequently, depleting RBM38c enhances the efficacy of DNA-damaging drugs by impairing autophagy and increasing DNA damage. Clinical lung cancer samples show a positive correlation between RBM38c expression and LC3 expression, and this correlation is linked to chemotherapy resistance. Together, our study reveals a novel mechanism for DNA damage-induced autophagy, involving K63-linked ubiquitination of RBM38c as a critical interactor with BECN1.
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