ArticleScience China. Life sciences2024
PCAF-mediated acetylation of METTL3 impairs mRNA translation efficiency in response to oxidative stress.
Article in Science China. Life sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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Who cites it
7 citing papers in PubMed.
- Research progress on lysine acetylation (Review).International journal of molecular medicine · 2026Review
- METTL3 regulates exocytosis independently of mScience advances · 2026Article
- WTAP mediated mScience China. Life sciences · 2026Article
- Epitranscriptomic regulation by m6A in immunity and autoimmune disorders: emerging mechanisms and clinical perspectives.Frontiers in immunology · 2026Review
- Magnetofection-mediated siRNA delivery ameliorates cartilage damage in Kashin-Beck diseaseTheranostics · 2026Article
- RNA Modification in Metabolism.MedComm · 2025Review
- METTL3 as a potential therapeutic target in gastric cancer.Frontiers in oncology · 2024Review
Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
METTL3 methylates RNA and regulates the fate of mRNA through its methyltransferase activity. METTL3 enhances RNA translation independently of its catalytic activity. However, the underlying mechanism is still elusive. Here, we report that METTL3 is both interacted with and acetylated at lysine 177 by the acetyltransferase PCAF and deacetylated by SIRT3. Neither the methyltransferase activity nor the stability of METTL3 is affected by its acetylation at K177. Importantly, acetylation of METTL3 blocks its interaction with EIF3H, a subunit of the translation initiation factor, thereby reducing mRNA translation efficiency. Interestingly, acetylation of METTL3 responds to oxidative stress. Mechanistically, oxidative stress enhances the interaction of PCAF with METTL3, increases METTL3 acetylation, and suppresses the interaction of METTL3 with EIF3H, thereby decreasing the translation efficiency of ribosomes and inhibiting cell proliferation. Altogether, we suggest a mechanism by which oxidative stress regulates RNA translation efficiency by the modulation of METTL3 acetylation mediated by PCAF.
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Identifiers
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Registered trials
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