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表观遗传学中的锌金属蛋白及其相互作用

Zinc Metalloproteins in Epigenetics and Their Crosstalk.

作者信息

Yusuf Abdurrahman Pharmacy, Abubakar Murtala Bello, Malami Ibrahim, Ibrahim Kasimu Ghandi, Abubakar Bilyaminu, Bello Muhammad Bashir, Qusty Naeem, Elazab Sara T, Imam Mustapha Umar, Alexiou Athanasios, Batiha Gaber El-Saber

机构信息

Centre for Advanced Medical Research and Training, Usmanu Danfodiyo University, P.M.B. 2346 Sokoto, Nigeria.

Department of Physiology, Faculty of Basic Medical Sciences, College of Health Sciences, Usmanu Danfodiyo University, P.M.B. 2254 Sokoto, Nigeria.

出版信息

Life (Basel). 2021 Feb 26;11(3):186. doi: 10.3390/life11030186.

DOI:10.3390/life11030186
PMID:33652690
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7996840/
Abstract

More than half a century ago, zinc was established as an essential micronutrient for normal human physiology. In silico data suggest that about 10% of the human proteome potentially binds zinc. Many proteins with zinc-binding domains (ZBDs) are involved in epigenetic modifications such as DNA methylation and histone modifications, which regulate transcription in physiological and pathological conditions. Zinc metalloproteins in epigenetics are mainly zinc metalloenzymes and zinc finger proteins (ZFPs), which are classified into writers, erasers, readers, editors, and feeders. Altogether, these classes of proteins engage in crosstalk that fundamentally maintains the epigenome's modus operandi. Changes in the expression or function of these proteins induced by zinc deficiency or loss of function mutations in their ZBDs may lead to aberrant epigenetic reprogramming, which may worsen the risk of non-communicable chronic diseases. This review attempts to address zinc's role and its proteins in natural epigenetic programming and artificial reprogramming and briefly discusses how the ZBDs in these proteins interact with the chromatin.

摘要

半个多世纪前,锌被确认为正常人体生理所必需的微量营养素。计算机模拟数据表明,人类蛋白质组中约10%的蛋白质可能与锌结合。许多具有锌结合结构域(ZBD)的蛋白质参与表观遗传修饰,如DNA甲基化和组蛋白修饰,这些修饰在生理和病理条件下调节转录。表观遗传学中的锌金属蛋白主要是锌金属酶和锌指蛋白(ZFP),它们被分为写入器、擦除器、读取器、编辑器和供给器。总之,这些蛋白质类别相互作用,从根本上维持着表观基因组的运作方式。锌缺乏或其ZBD功能丧失突变导致这些蛋白质的表达或功能改变,可能会导致异常的表观遗传重编程,这可能会增加非传染性慢性病的风险。本文综述试图阐述锌及其相关蛋白质在自然表观遗传编程和人工重编程中的作用,并简要讨论这些蛋白质中的ZBD如何与染色质相互作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/507d/7996840/9dd10ace6e00/life-11-00186-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/507d/7996840/1a4963537cef/life-11-00186-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/507d/7996840/7a94465a6342/life-11-00186-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/507d/7996840/8326455a46c6/life-11-00186-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/507d/7996840/8af160e4d76e/life-11-00186-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/507d/7996840/9dd10ace6e00/life-11-00186-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/507d/7996840/1a4963537cef/life-11-00186-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/507d/7996840/7a94465a6342/life-11-00186-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/507d/7996840/8326455a46c6/life-11-00186-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/507d/7996840/8af160e4d76e/life-11-00186-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/507d/7996840/9dd10ace6e00/life-11-00186-g005.jpg

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本文引用的文献

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Nutr Neurosci. 2022 May;25(5):1001-1010. doi: 10.1080/1028415X.2020.1831259. Epub 2020 Oct 20.
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Acetylated histone H4 tail enhances histone H3 tail acetylation by altering their mutual dynamics in the nucleosome.乙酰化组蛋白 H4 尾部通过改变核小体中它们的相互动态,增强了组蛋白 H3 尾部的乙酰化。
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Methylation-associated silencing of miR-193b improves the radiotherapy sensitivity of esophageal cancer cells by targeting cyclin D1 in areas with zinc deficiency.
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Sci Rep. 2025 Jan 22;15(1):2749. doi: 10.1038/s41598-025-85410-7.
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Deletion of metal transporter Zip14 reduces major histocompatibility complex II expression in murine small intestinal epithelial cells.金属转运蛋白Zip14的缺失降低了小鼠小肠上皮细胞中主要组织相容性复合体II的表达。
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Cellular zinc status alters chromatin accessibility and binding of p53 to DNA.细胞内锌的状态改变了染色质的可及性以及 p53 与 DNA 的结合。
Life Sci Alliance. 2024 Jul 5;7(9). doi: 10.26508/lsa.202402638. Print 2024 Sep.
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Sex-specific epigenetics drive low GPER expression in gastrointestinal smooth muscles in type 2 diabetic mice.性别特异性表观遗传学导致 2 型糖尿病小鼠胃肠道平滑肌中 GPER 表达降低。
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Modulation of the Gut Microbiota by Nutrition and Its Relationship to Epigenetics.营养对肠道微生物群的调节及其与表观遗传学的关系。
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