Special Issue "The Role of Methylation in the Modulation of Intracellular Signaling Pathways"

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cell Signaling".

Deadline for manuscript submissions: 31 December 2023 | Viewed by 310

Special Issue Editors

West China School of Medicine, Sichuan University, Chengdu, China
Interests: oncogenesis; chemoresistance; gene transcription; autophagy; nucleosome assembly
Dr. Gang Yuan
E-Mail Website
Guest Editor
West China School of Medicine, Sichuan University, Chengdu, China
Interests: tumorigenesis; histone modifications; histone variants; chromatin remodeling; transcriptional regulation; non-histone methylation

Special Issue Information

Dear Colleagues,

To respond to an external stimulus, cells take a basic action named intracellular signaling, which is functioning in most biological processes, such as normal development and pathogenesis. While classical signaling cascade is best exemplified with activation by phosphorylation on key proteins in a specific pathway, other types of post-translational modifications, such as methylation, are also involved in the modulation of intracellular signaling pathways.

Methylation on histone proteins has been extensively studied over the past two decades and such methylation directly regulates gene expression and plays important roles in various signaling pathways. In recent years, research has gradually shed light on the role of methylation on non-histone proteins, especially important signaling mediators. Dysregulation of such methylation events also leads to diseases, including cancer.

In addition to proteins, nucleic acids are also important subjects of methylation. DNA methylation has long been indicated to play important roles in early development, while the derivates of DNA methylation, such as DNA hydroxymethylation, are also reported to be involved in neuronal differentiation. Compared with DNA methylation, RNA methylation is much more complex, and different RNA species, including mRNA, tRNA and rRNA, can be extensively methylated and the methylation occurs at different ribonucleotides, such as adenine (A), cytosine (C) and guanine (G). In particular, great progress has been made towards the function and working mechanism of m6A on mRNA, including its role in various signaling pathways.

This research topic aims to present the latest research on the role of methylation in modulating intracellular signaling pathways, either in normal development or during pathogenesis. We welcome original research and reviews that explore, but are not limited to, the following list of themes:

  • Methylation of histone proteins in modulating intracellular signaling pathways
  • Methylation of non-histone proteins in modulating intracellular signaling pathways
  • Methylation of DNA in modulating intracellular signaling pathways
  • Methylation of RNA in modulating intracellular signaling pathways
  • Methylation of histone, DNA and RNA involved in cancer intracellular signaling pathways.

Dr. Junhong Han
Dr. Gang Yuan
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.


  • methylation
  • histone
  • DNA
  • RNA
  • cancer
  • signaling pathway

Published Papers

This special issue is now open for submission, see below for planned papers.

Planned Papers

The below list represents only planned manuscripts. Some of these manuscripts have not been received by the Editorial Office yet. Papers submitted to MDPI journals are subject to peer-review.

Title: Inflammation and DNA methylation in Alzheimer’s disease: how immune cell oxidants influence the aging brain.
Authors: Seddon, A.R; MacArthur, C; Thunders, M; Hampton MB; Stevens A.J
Affiliation: University of Otago, Christchurch, Department of Pathology and Biomedical Science, Christchurch, New Zealand University of Otago, Wellington, Department of Pathology and Molecular Medicine, Wellington, New Zealand
Abstract: Alzheimer’s disease (AD) is a neurodegenerative disease involving memory impairment, confusion, and behavioural changes. AD is characterized by the accumulation of amyloid β plaques and neurofibrillary tangles in the brain which disrupt normal neuronal function. There is no known cure for AD and due to increasing life expectancy, it is projected that cases will rise over the coming decades. The causes of the disorder are multifactorial with inflammation, oxidative stress, genetic and epigenetic variation, and cerebrovascular abnormalities among the strongest contributors. In this review we will provide an overview of the current literature surrounding inflammation and epigenetics in AD, with a focus on how oxidants from infiltrating immune cells have the potential to alter DNA methylation profiles in the aging brain, highlighting a novel mechanism for Alzheimer’s disease pathology.

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