Evaluation of post-translational modifications in histone proteins: A review on histone modification defects in developm
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Review Evaluation of post-translational modifications in histone proteins: A review on histone modification defects in developmental and neurological disorders SHAHIN RAMAZI1, ABDOLLAH ALLAHVERDI1*
and JAVAD ZAHIRI2
1
Department of Biophysics, Faculty of Biological Sciences, Tarbiat Modares University, Jalal Ale Ahmad Highway, P.O. Box: 14115-111, Tehran, Iran
2
Bioinformatics and Computational Omics Lab (BioCOOL), Department of Biophysics, Faculty of Biological Sciences, Tarbiat Modares University, Jalal Ale Ahmad Highway, P.O. Box: 14115-111, Tehran, Iran *Corresponding author (Email, [email protected]) MS received 2 March 2020; accepted 14 September 2020
Post-translational modification (PTM) in histone proteins is a covalent modification which mainly consists of methylation, phosphorylation, acetylation, ubiquitylation, SUMOylation, glycosylation, and ADP-ribosylation. PTMs have fundamental roles in chromatin structure and function. Histone modifications have also been known as epigenetic markers. The PTMs that have taken place in histone proteins can affect gene expression by altering chromatin structure. Histone modifications act in varied biological processes such as transcriptional activation/inactivation, chromosome packaging, mitosis, meiosis, apoptosis, and DNA damage/repair. Defects in the PTMs pathway have been associated with the occurrence and progression of various human diseases, such as cancer, heart failure, autoimmune diseases, and neurodegenerative disorders such as Parkinson’s disease, Alzheimer’s disease, and Huntington’s disease. Histone modifications are reversible and used as potential targets for cancer therapy and prevention. Recent different histone PTMs have key roles in cancer cells since it has been shown that histone PTMs markers in cancers are acetylation, methylation, phosphorylation, and ubiquitylation. In this review, we have summarized the six most studied histone modifications and have examined the role of these modifications in the development of cancer. Keywords.
Chromatin; disease; histone proteins; histone modifications; post-translational modifications
Abbreviations: ADP, adenosine diphosphate; ADP-ribose, adenosine diphosphate ribose; ART, ADPribosyltransferases; ARTD1/ PARP1, poly [ADP-ribose] polymerase 1; ATM/ATR, ATM/ATR serine/threonine kinase; ATP, adenosine triphosphate; BRCA1, breast cancer type 1 susceptibility protein; CARM1, coactivatorassociated arginine methyltransferase 1; ChIP, combines chromatin immunoprecipitation; ChIP-seq, ChIPsequencing; CRC, colorectal cancer; DMFS, distant metastasis-free survival; DNase I, deoxyribonuclease I; DSBs, DNA double-strand breaks; E1, ubiquitin/sumo activating; E2, ubiquitin/sumo conjugating; E3, ubiquitin/sumo ligase; EZH2, Zeste homolog 2; HATs, histone acetyltransferases; HDAC, histone deacetylase; HMTs, histone methyltransferases; HP1, heterochromatin protein; LSD1, lysine-specific histone demethyla1; MAP kinase, mitogen-activated protein k
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