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Int. J. Mol. Sci. 2018, 19(8), 2345; https://doi.org/10.3390/ijms19082345

N6-Methyladenosine Role in Acute Myeloid Leukaemia

Department of Biology and Biotechnology “Charles Darwin”, Sapienza University of Rome, 00185 Rome, Italy
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Received: 30 July 2018 / Revised: 7 August 2018 / Accepted: 8 August 2018 / Published: 9 August 2018
(This article belongs to the Special Issue Feature Annual Reviews in Molecular Sciences 2019)
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Abstract

We are currently assisting in the explosion of epitranscriptomics, which studies the functional role of chemical modifications into RNA molecules. Among more than 100 RNA modifications, the N6-methyladenosine (m6A), in particular, has attracted the interest of researchers all around the world. m6A is the most abundant internal chemical modification in mRNA, and it can control any aspect of mRNA post-transcriptional regulation. m6A is installed by “writers”, removed by “erasers”, and recognized by “readers”; thus, it can be compared to the reversible and dynamic epigenetic modifications in histones and DNA. Given its fundamental role in determining the way mRNAs are expressed, it comes as no surprise that alterations to m6A modifications have a deep impact in cell differentiation, normal development and human diseases. Here, we review the proteins involved in m6A modification in mammals, m6A role in gene expression and its contribution to cancer development. In particular, we will focus on acute myeloid leukaemia (AML), which provides an initial indication of how alteration in m6A modification can disrupt normal cellular differentiation and lead to cancer. View Full-Text
Keywords: m6A; RNA; AML; leukaemia; epitranscriptomics m6A; RNA; AML; leukaemia; epitranscriptomics
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This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).
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Ianniello, Z.; Fatica, A. N6-Methyladenosine Role in Acute Myeloid Leukaemia. Int. J. Mol. Sci. 2018, 19, 2345.

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