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nature portfolio privacy policy aff4/nf-κb/myc signaling network yolk-sac-derived erythro-myeloid progenitors national key research targeting fto/m6a/myc/cebpa signaling247 advertising targeting fto/ma/myc/cebpa signaling il-7/stat5/socs signaling pathways42 kdm4c-alkbh5-axl signaling axis full size table social media translational research east asian populations214 east asian populations r-2hg-sensitive aml cells body mass index reprints human hnrnp a2/b1 steroidal anti-inflammatory drug hnrnp a2/b1 knockdown neural stem/progenitor cells stimulating nf-κb pathway post-transcriptional regulatory markers coding rna hif1a-as2 mouse pre-implantation development hematopoietic stem/progenitor cells accelerating pri-mir221/222 maturation rna n6-methyladenosine methyltransferase n6-methyladenosine-encoded epitranscriptomics arginine-rich splicing factors n-methyladenosine binding protein rna-binding protein hur endogenous double-stranded rnas a-cdcp1 signaling axis rna n6-methyladenosine modification applying m6a-ref-seq n-methyladenosine-modified rna mrna n6-methyladenosine methylation leukaemia stem-cell development methyladenosine-mediated decay drives canonical rna-binding domains retroviral-mediated gene transfer targeted m6a-modified transcripts reduced rna-binding capability durable neoantigen-specific immunity bcr-abl1 fusion protein246 antibody-independent quantitative profiling activate pi3k/akt pathway /r-treated cardiomyocytes dependent

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         description:N6-methyladenosine (m6A) is the most prevalent, abundant and conserved internal cotranscriptional modification in eukaryotic RNAs, especially within higher eukaryotic cells. m6A modification is modified by the m6A methyltransferases, or writers, such as METTL3/14/16, RBM15/15B, ZC3H3, VIRMA, CBLL1, WTAP, and KIAA1429, and, removed by the demethylases, or erasers, including FTO and ALKBH5. It is recognized by m6A-binding proteins YTHDF1/2/3, YTHDC1/2 IGF2BP1/2/3 and HNRNPA2B1, also known as “readers”. Recent studies have shown that m6A RNA modification plays essential role in both physiological and pathological conditions, especially in the initiation and progression of different types of human cancers. In this review, we discuss how m6A RNA methylation influences both the physiological and pathological progressions of hematopoietic, central nervous and reproductive systems. We will mainly focus on recent progress in identifying the biological functions and the underlying molecular mechanisms of m6A RNA methylation, its regulators and downstream target genes, during cancer progression in above systems. We propose that m6A RNA methylation process offer potential targets for cancer therapy in the future.
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      name:Kunming Medical University, Kunming, China
      name:Key Laboratory of Animal Models and Human Disease Mechanisms of Chinese Academy of Sciences & Yunnan Province, Kunming Institute of Zoology, Kunming, China
      name:Key Laboratory of Animal Models and Human Disease Mechanisms of Chinese Academy of Sciences & Yunnan Province, Kunming Institute of Zoology, Kunming, China
      name:Center for Excellence in Animal Evolution and Genetics, Chinese Academy of Sciences, Kunming, China

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