ArticleJournal of translational medicine2021
ALKBH3 partner ASCC3 mediates P-body formation and selective clearance of MMS-induced 1-methyladenosine and 3-methylcytosine from mRNA.
Article in Journal of translational medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 24 citations in OpenAlex.
- Steaming and Sodium Bicarbonate-Assisted Aqueous Extraction ofFoods (Basel, Switzerland) · 2026Article
- tRNA synthetase activity is required for stress granule and P-body assembly.Genes & development · 2026Article
- tRNA mCellular & molecular immunology · 2026Article
- Therapy-induced mRNA, rRNA and tRNA methylation alterations confer tolerance phenotype in tumor cells: mechanism and implications.International journal of biological sciences · 2026Review
- RNA sculpting by the primordial Helix-clasp-Helix-Strand-Loop (HcH-SL) motif enforces chemical recognition enabling diverse KH domain functions.The Journal of biological chemistry · 2025Review
- Epitranscriptomic control of cancer immunity and therapy resistance.Frontiers in immunology · 2025Review
- Oligomerization regulates the interaction of Gemin5 with members of the SMN complex and the translation machinery.Cell death discovery · 2024Article
- Structural Basis of Nucleic Acid Recognition and 6mA Demethylation byInternational journal of molecular sciences · 2024Article
- ASCC3 promotes the immunosuppression and progression of non-small cell lung cancer by impairing the type I interferon response via CAND1-mediated ubiquitination inhibition of STAT3.Journal for immunotherapy of cancer · 2023Article
- How RNA impacts DNA repair.DNA repair · 2023Review
- Extended DNA threading through a dual-engine motor module of the activating signal co-integrator 1 complex.Nature communications · 2023Article
- Expression pattern, tumor immune landscape, and prognostic value of N7‑methylguanosine regulators in bladder urothelial carcinoma.Oncology letters · 2023Article
- Functional and structural deficiencies of Gemin5 variants associated with neurological disorders.Life science alliance · 2022Article
- Phosphorylation of T897 in the dimerization domain of Gemin5 modulates protein interactions and translation regulation.Computational and structural biotechnology journal · 2022Article
- Construction and Validation of a m7G-Related Gene-Based Prognostic Model for Gastric Cancer.Frontiers in oncology · 2022Article
- Current Advances in N6-Methyladenosine Methylation Modification During Bladder Cancer.Frontiers in genetics · 2021Review
- Understanding GEMIN5 Interactions: From Structural and Functional Insights to Selective Translation.Wiley interdisciplinary reviews. RNAReview
Corrections and comments
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Authors and funding
14 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundReversible enzymatic methylation of mammalian mRNA is widespread and serves crucial regulatory functions, but little is known to what degree chemical alkylators mediate overlapping modifications and whether cells distinguish aberrant from canonical methylations.
methodsHere we use quantitative mass spectrometry to determine the fate of chemically induced methylbases in the mRNA of human cells. Concomitant alteration in the mRNA binding proteome was analyzed by SILAC mass spectrometry.
resultsMMS induced prominent direct mRNA methylations that were chemically identical to endogenous methylbases. Transient loss of 40S ribosomal proteins from isolated mRNA suggests that aberrant methylbases mediate arrested translational initiation and potentially also no-go decay of the affected mRNA. Four proteins (ASCC3, YTHDC2, TRIM25 and GEMIN5) displayed increased mRNA binding after MMS treatment. ASCC3 is a binding partner of the DNA/RNA demethylase ALKBH3 and was recently shown to promote disassembly of collided ribosomes as part of the ribosome quality control (RQC) trigger complex. We find that ASCC3-deficient cells display delayed removal of MMS-induced 1-methyladenosine (m
conclusionsOur findings conform to a model in which ASCC3-mediated disassembly of collided ribosomes allows demethylation of aberrant m
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