首页 产品 化合物库 服务 Kit 关于我们 联系我们

信号通路

在线客服 在线询单 如何订购 促销产品 销售网络 定制服务

在线询价

温馨提示:客服在线时为9:00-18:00,
其他时间可发邮件至sales@medchemexpress.cn,我们会尽快回复您。

表观遗传学

Epigenetic mechanisms involve heritable changes in gene expression that are not linked to the alteration of DNA sequence. Epigenetically active compounds that influence activity of epigenetic modulators such as DNA methyltransferases (DNMTs), histone acetyltransferases, histone deacetylases (HDACs), etc. may correct these pathogenic changes in the epigenome and therefore be used for Cardiovascular disease (CVD) therapy. Epigenetic mechanisms such as DNA methylation and histone modifications in cardiovascular pathology and the epigenetics-based therapeutic approaches focused on the implementation of DNMT and HDAC inhibitors[1].

All epigenetic processes are mediated by protein complexes that either mediate specific DNA methylation patterns, or modify nucleosomal proteins in a covalent fashion (acetylation, methylation, phosphorylation and ubiquitinylation). One important player involved in epigenetics is the mixed lineage leukemia (MLL) protein which represents a histone H3 methyltransferase[2]

Epigenetic modifications sit 'on top of' the genome and influence DNA transcription, which can force a significant impact on cellular behavior and phenotype and, consequently human development and disease[3]

MicroRNAs (miRNAs) are highly conserved elements in mammals, and exert key regulatory functions. MicroRNAs can interact with another class of non-coding RNAs, so-called transcribed ultraconserved regions (T-UCRs), which take part in transcriptional, post-transcriptional and epigenetic regulation processes[4].

References:

[1] Chistiakov DA, et al. Treatment of cardiovascular pathology with epigenetically active agents: Focus on natural and synthetic inhibitors of DNA methylation and histone deacetylation. Int J Cardiol. 2017 Jan 15;227:66-82.

[2] Rössler T,  et al. An alternative splice process renders the MLL protein either into a transcriptional activator or repressor. Pharmazie. 2013 Jul;68(7):601-7.

[3] Ma Y, et al. Chiral Antioxidant-based Gold Nanoclusters Reprogram DNA Epigenetic Patterns. Sci Rep. 2016 Sep 16;6:33436.

[4] Terreri S, et al. New Cross-Talk Layer between Ultraconserved Non-Coding RNAs, MicroRNAs and Polycomb Protein YY1 in Bladder Cancer. Genes (Basel). 2016 Dec 14;7(12). pii: E127.

 
Epigenetics通路中的靶点

关键字:表观遗传学 | 表观遗传学 抑制剂 | 表观遗传学 激动剂 | 表观遗传学 抑制 | 表观遗传学 激活 | 表观遗传学 药物靶点 | 表观遗传学 活性 | 表观遗传学 信号通路 | 表观遗传学 作用机制 | 表观遗传学 抑制剂治疗 | 表观遗传学 抑制剂筛选 | 表观遗传学 口服抑制剂 | 表观遗传学 抑制剂综述 | 表观遗传学 抑制剂列表 | 表观遗传学 特异性抑制剂 | 表观遗传学 不可逆抑制剂 |表观遗传学 FDA上市抑制剂 | 表观遗传学 抑制剂供应商 | 表观遗传学 抑制剂分销商

SiteMap

MCE所有的产品和服务只应用于科学研究,我们不提供产品和服务给任何个人。

Copyright © 2013-2014 MedChemexpress All Rights Reserved 沪ICP备15051369号-1