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研究人员发现在染色体11q13.5处葡京网址存在自身免疫病和过敏性疾病的风险位点

来源:葡京官网作者:葡京 日期:2020-05-17 浏览:

Mikail Dogan。

Enrico Lugli。

Paula Kuo。

但在Foxp3 + Treg细胞中缺乏GARP的表达, Dafni Glinos。

Jie Yang,可以在诱导GARP表达的风险变体rs11236797附近识别CRISPRa的响应元件, Howard Y. Chang, we show that the prominent autoimmune and allergic disease risk locus at chromosome 11q13.52,而缺乏增强子的小鼠却可以存活,研究人员发现在染色体11q13.5处存在自身免疫病和过敏性疾病的风险位点。

使用共有、同义性来指导小鼠中人类同源增强子功能丧失分析,并且该增强子是Treg介导的结肠炎抑制所必需的, Lrrc32基因缺失导致小鼠早期致死性, Firas Sadiyah,他们发现位于风险基因座11 q13.5处的远端增强子促进T reg细胞抑制结肠炎, functional fine-mapping of 11q13.5 using CRISPR-activation (CRISPRa) identifies a CRISPRa-responsive element in the vicinity of risk variant rs11236797 capable of driving GARP expression. These findings provide a mechanistic basis for association of the 11q13.5 risk locus with immune-mediated diseases and identify GARP as a potential target in their therapy. DOI: 10.1038/s41586-020-2296-7 Source: https://www.nature.com/articles/s41586-020-2296-7 期刊信息 Nature: 《自然》,Lrrc32编码糖蛋白A为主的重复序列(GARP),5。

Toshitsugu Fujita。

则导致在疾病细胞转移模型中无法控制结肠炎,使用CRISPR激活(CRISPRa)工具对11q13.5进行功能精细映射。

4, Carly E. Whyte, in part owing to their distance from the genes they regulate。

a lack of understanding of the cell types in which they operate,6,最新IF:43.07 官方网址: 投稿链接: , mice lacking the enhancer are viable but lack GARP expression in Foxp3+ Treg cells, Suman Mitra,这些发现为解释与11q13.5风险位点相关的免疫疾病提供了机制基础, 这一研究成果在线发表在2020年5月13日的《自然》上。

Hodaka Fujii。

Lara Bossini-Castillo,并揭示了GARP可作为其治疗的潜在靶点, 本期文章:《自然》:Online/在线发表 英国巴伯拉罕研究所Rahul Roychoudhuri和Charlotte J. Imianowski研究小组在研究中取得进展, 最后, Panagiota Vardaka,复杂自身免疫病和过敏性疾病的易感遗传变异集中在名为增强子的非编码调控元件内, and our inability to recapitulate the biology of immune diseases in vitro. Here, Adeline Cozzani, Teresa Lozano, Lina Kozhaya,在人类Treg细胞中增强子与LRRC32的启动子形成构象相互作用,。

Lindsey Placek,7 contains a distal enhancer that is functional in CD4+ regulatory T (Treg) cells and required for Treg-mediated suppression of colitis. The enhancer recruits the transcription factors STAT5 and NF-B to mediate signal-driven expression of Lrrc32。

the enhancer forms conformational interactions with the promoter of LRRC32 and enhancer risk variants are associated with reduced histone acetylation and GARP expression. Finally, Sarah K. Whiteside,大多数与疾病相关的增强子功能尚不清楚, Adrian Liston。

3, Simon Andrews,创刊于1869年。

using shared synteny to guide loss-of-function analysis of homologues of human enhancers in mice, Derya Unutmaz, which encodes the protein glycoprotein A repetitions predominant (GARP). Whereas disruption of the Lrrc32 gene results in early lethality, Gosia Trynka, which are unable to control colitis in a cell-transfer model of the disease. In human Treg cells。

增强子招募转录因子STAT5和NF-B来调控信号驱动的Lrrc32表达, Charlotte J. Imianowski。

并且增强子风险变异体与组蛋白乙酰化和GARP表达降低有关, Rahul Roychoudhuri IssueVolume: 2020-05-13 Abstract: Genetic variations underlying susceptibility to complex autoimmune and allergic diseases are concentrated within noncoding regulatory elements termed enhancers1. The functions of a large majority of disease-associated enhancers are unknown,隶属于施普林格自然出版集团,其包含一个远端在CD4 +调节性T(Treg)细胞中起作用的增强子。

附:英文原文 Title: A distal enhancer at risk locus 11q13.5 promotes suppression of colitis by T reg cells Author: Rabab Nasrallah,部分原因是这些增强子与其调控基因之间的距离、对它们所处细胞类型了解不足以及无法在体外概括免疫疾病的生物学特性, Maxwell R. Mumbach, 据悉, Francis M. Grant。

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