Biology

Journal Browser

► Journal Browser

Molecular Mechanism of Histone Modification and Gene Regulation

Share This Special Issue

Special Issue Information

Dear Colleagues,

Histones undergo a variety of post-translational modifications (PTMs) including acetylation, methylation, phosphorylation, and ubiquitylation, among numerous others. These PTMs can impact gene expression by altering chromatin structure or recruiting reader proteins. Aberrant histone modifications are linked to the pathogenesis of diseases such as cancers as well as inflammatory and metabolic diseases. Thus, elucidating the molecular mechanisms by which histone modifications regulate gene expression is critical to understanding disease development.

This Special Issue invites original articles and reviews focusing on the broad topic of histone modifications and gene regulation related to cell differentiation, environmental stress, and human disease.

Dr. Kyunghwan Kim
Dr. Kwang Won Jeong
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. Biology is an international peer-reviewed open access monthly 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.

Keywords

nucleosome
histone modification
gene expression
chromatin
cell differentiation
environmental stress
human disease

Published Papers (2 papers)

Download All Papers

Research

Jump to: Review

13 pages, 2754 KiB

Open AccessFeature PaperArticle

Transcriptome Analysis Reveals That Abeliophyllum distichum Nakai Extract Inhibits RANKL-Mediated Osteoclastogenensis Mainly through Suppressing Nfatc1 Expression

by Kyubin Lee, You-Jee Jang, Hyerim Lee, Eunbin Kim, Yeojin Kim, Tong-Kewn Yoo, Tae Kyung Hyun, Jae-Il Park, Sun-Ju Yi and Kyunghwan Kim

Biology 2020, 9(8), 212; https://0-doi-org.brum.beds.ac.uk/10.3390/biology9080212 - 06 Aug 2020

Cited by 9 | Viewed by 2775

Abstract

Abeliophyllum distichum Nakai is known as a monotypic genus endemic to South Korea. Currently, several pharmacological studies have revealed that A. distichum extract exhibits diverse biological functions, including anti-cancer, anti-diabetic, anti-hypertensive, and anti-inflammatory activities. In this study, we present the anti-osteoporotic activity of A. distichum extract by inhibiting osteoclast formation. First, we show that the methanolic extract of the leaves of A. distichum, but not extracts of the branches or fruits, significantly inhibits receptor activator of the NF-κB ligand (RANKL)-induced osteoclast differentiation. Second, our transcriptome analysis revealed that the leaf extract (LE) blocks sets of RANKL-mediated osteoclast-related genes. Third, the LE attenuates the phosphorylation of extracellular signal-related kinase. Finally, treatment with the LE effectively prevents postmenopausal bone loss in ovariectomized mice and glucocorticoid-induced osteoporosis in zebrafish. Our findings show that the extract of A. distichum efficiently suppressed osteoclastogenesis by regulating osteoclast-related genes, thus offering a novel therapeutic strategy for osteoporosis. Full article

(This article belongs to the Special Issue Molecular Mechanism of Histone Modification and Gene Regulation)

► Show Figures

Figure 1

Review

Jump to: Research

32 pages, 10485 KiB

Open AccessReview

Histone H3K4 Methyltransferases as Targets for Drug-Resistant Cancers

by Liu Yang, Mingli Jin and Kwang Won Jeong

Biology 2021, 10(7), 581; https://0-doi-org.brum.beds.ac.uk/10.3390/biology10070581 - 25 Jun 2021

Cited by 19 | Viewed by 3388

Abstract

The KMT2 (MLL) family of proteins, including the major histone H3K4 methyltransferase found in mammals, exists as large complexes with common subunit proteins and exhibits enzymatic activity. SMYD, another H3K4 methyltransferase, and SET7/9 proteins catalyze the methylation of several non-histone targets, in addition to histone H3K4 residues. Despite these structural and functional commonalities, H3K4 methyltransferase proteins have specificity for their target genes and play a role in the development of various cancers as well as in drug resistance. In this review, we examine the overall role of histone H3K4 methyltransferase in the development of various cancers and in the progression of drug resistance. Compounds that inhibit protein–protein interactions between KMT2 family proteins and their common subunits or the activity of SMYD and SET7/9 are continuously being developed for the treatment of acute leukemia, triple-negative breast cancer, and castration-resistant prostate cancer. These H3K4 methyltransferase inhibitors, either alone or in combination with other drugs, are expected to play a role in overcoming drug resistance in leukemia and various solid cancers. Full article

(This article belongs to the Special Issue Molecular Mechanism of Histone Modification and Gene Regulation)

► Show Figures