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Coordinated methyl readers: Functional communications in cancer

Authors
Park, Il-GeunJeon, MinsolKim, HyunkyungLee, Ji Min
Issue Date
Aug-2022
Publisher
Academic Press
Keywords
Chromodomain; Epigenetics; Methyl reader; PHD; Tudor
Citation
Seminars in Cancer Biology, v.83, pp.88 - 99
Indexed
SCIE
SCOPUS
Journal Title
Seminars in Cancer Biology
Volume
83
Start Page
88
End Page
99
URI
https://scholarworks.korea.ac.kr/kumedicine/handle/2020.sw.kumedicine/52976
DOI
10.1016/j.semcancer.2021.03.015
ISSN
1044-579X
Abstract
Methylation is a major post-translational modification (PTM) generated by methyltransferase on target proteins; it is recognized by the epigenetic reader to expand the functional diversity of proteins. Methylation can occur on specific lysine or arginine residues localized within regulatory domains in both histone and nonhistone proteins, thereby allowing distinguished properties of the targeted protein. Methylated residues are recognized by chromodomain, malignant brain tumor (MBT), Tudor, plant homeodomain (PHD), PWWP, WD-40, ADD, and ankyrin repeats by an induced-fit mechanism. Methylation-dependent activities regulate distinct aspects of target protein function and are largely reliant on methyl readers of histone and nonhistone proteins in various diseases. Methylation of nonhistone proteins that are recognized by methyl readers facilitates the degradation of unwanted proteins, as well as the stabilization of necessary proteins. Unlike nonhistone substrates, which are mainly monomethylated by methyltransferase, histones are di- or trimethylated by the same methyltransferases and then connected to other critical regulators by methyl readers. These fine-tuned controls by methyl readers are significant for the progression or inhibition of diseases, including cancers. Here, current knowledge and our perspectives about regulating protein function by methyl readers are summarized. We also propose that expanded research on the strong crosstalk mechanisms between methylation and other PTMs via methyl readers would augment therapeutic research in cancer. © 2021 The Author(s)
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