ArticleNature communications2016
YTHDF2 destabilizes m(6)A-containing RNA through direct recruitment of the CCR4-NOT deadenylase complex.
Article in Nature communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 994 papers.
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Who cites it
994 citing papers in PubMed, 1,504 citations in OpenAlex.
- Article
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- Polyphenism Through RNA Chemical Modifications.Molecular ecology · 2026Review
- Global Regulatory Functions of the Human CCR4-NOT Complex in mRNA Deadenylation and Decay.bioRxiv : the preprint server for biology · 2026Article
- FTO Deficiency Inhibits Vascular Endothelial Cell Apoptosis and Improved Mitophagy in Obesity-Related Hypertension by Enhancing NDRG1 m6A Methylation.Biochemical genetics · 2026Article
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- METTL14 Promotes Chicken Preadipocyte Differentiation by Modulating mRNA Stability via a Dual-Reader mCells · 2026Article
- The stability of m6A-marked transcripts is linked to cell identity in planarians.Nucleic acids research · 2026Article
- Interaction between N6-methyladenosine (mGenes & diseases · 2026Review
- The mitochondria enzyme OGDH defends against disulfidptosis by licensing METTL3-regulated NRF2 translation.Nature cell biology · 2026Article
- Characterization of METTL3/14-mediated m6A modification in human transcriptome using Nanopore direct RNA sequencing.PLoS genetics · 2026Article
- mNature reviews. Neuroscience · 2026Review
- Precision in RNA degradation: helicases, ribosome and RNA polymerase stalling, and RNA modifications.Trends in cell biology · 2026Review
- The m⁶A reader YTHDF2 regulates mRNA transport and axon outgrowth in developing neurons.Nature communications · 2026Article
- Role and prognostic value of N6-methyladenosine RNA modification regulators in glycolytic reprogramming during sepsis.Journal of intensive care · 2026Article
934 more citing papers are in PubMed but not listed here.
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Authors and funding
8 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Methylation at the N6 position of adenosine (m(6)A) is the most abundant RNA modification within protein-coding and long noncoding RNAs in eukaryotes and is a reversible process with important biological functions. YT521-B homology domain family (YTHDF) proteins are the readers of m(6)A, the binding of which results in the alteration of the translation efficiency and stability of m(6)A-containing RNAs. However, the mechanism by which YTHDF proteins cause the degradation of m(6)A-containing RNAs is poorly understood. Here we report that m(6)A-containing RNAs exhibit accelerated deadenylation that is mediated by the CCR4-NOT deadenylase complex. We further show that YTHDF2 recruits the CCR4-NOT complex through a direct interaction between the YTHDF2 N-terminal region and the SH domain of the CNOT1 subunit, and that this recruitment is essential for the deadenylation of m(6)A-containing RNAs by CAF1 and CCR4. Therefore, we have uncovered the mechanism of YTHDF2-mediated degradation of m(6)A-containing RNAs in mammalian cells.
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