Global S&T Development Trend Analysis Platform of Resources and Environment
DOI | 10.1126/science.aan0814 |
C1orf106 is a colitis risk gene that regulates stability of epithelial adherens junctions | |
Mohanan, Vishnu1,2; Nakata, Toru1,2; Desch, A. Nicole1,2; Levesque, Chloe3; Boroughs, Angela2; Guzman, Gaelen1; Cao, Zhifang2; Creasey, Elizabeth2; Yao, Junmei2; Boucher, Gabrielle3; Charron, Guy3; Bhan, Atul K.4,5,6; Schenone, Monica1; Carr, Steven A.1; Reinecker, Hans-Christian6,7; Daly, Mark J.1,5,6,8; Rioux, John D.3,9; Lassen, Kara G.1,2; Xavier, Ramnik J.1,2,6,7,10 | |
2018-03-09 | |
发表期刊 | SCIENCE |
ISSN | 0036-8075 |
EISSN | 1095-9203 |
出版年 | 2018 |
卷号 | 359期号:6380页码:1161-+ |
文章类型 | Article |
语种 | 英语 |
国家 | USA; Canada |
英文摘要 | Polymorphisms in C1orf106 are associated with increased risk of inflammatory bowel disease (IBD). However, the function of C1orf106 and the consequences of disease-associated polymorphisms are unknown. Here we demonstrate that C1orf106 regulates adherens junction stability by regulating the degradation of cytohesin-1, a guanine nucleotide exchange factor that controls activation of ARF6. By limiting cytohesin-1-dependent ARF6 activation, C1orf106 stabilizes adherens junctions. Consistent with this model, C1orf106(-/-) mice exhibit defects in the intestinal epithelial cell barrier, a phenotype observed in IBD patients that confers increased susceptibility to intestinal pathogens. Furthermore, the IBD risk variant increases C1orf106 ubiquitination and turnover with consequent functional impairments. These findings delineate a mechanism by which a genetic polymorphism fine-tunes intestinal epithelial barrier integrity and elucidate a fundamental mechanism of cellular junctional control. |
领域 | 地球科学 ; 气候变化 ; 资源环境 |
收录类别 | SCI-E |
WOS记录号 | WOS:000426835900047 |
WOS关键词 | INFLAMMATORY-BOWEL-DISEASE ; NUCLEOTIDE EXCHANGE FACTORS ; F-BOX PROTEINS ; PATHOGENESIS ; FAMILY ; PERMEABILITY ; CANCER ; ROLES ; LOCI |
WOS类目 | Multidisciplinary Sciences |
WOS研究方向 | Science & Technology - Other Topics |
URL | 查看原文 |
引用统计 | |
文献类型 | 期刊论文 |
条目标识符 | http://119.78.100.173/C666/handle/2XK7JSWQ/198154 |
专题 | 地球科学 资源环境科学 气候变化 |
作者单位 | 1.Broad Inst MIT & Harvard, Cambridge, MA 02142 USA; 2.Massachusetts Gen Hosp, Ctr Computat & Integrat Biol, Boston, MA 02114 USA; 3.Montreal Heart Inst, Res Ctr, Montreal, PQ H1T 1C8, Canada; 4.Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA; 5.Harvard Med Sch, Boston, MA 02114 USA; 6.Massachusetts Gen Hosp, Ctr Study Inflammatory Bowel Dis, Boston, MA 02114 USA; 7.Massachusetts Gen Hosp, Gastrointestinal Unit, Boston, MA 02114 USA; 8.Massachusetts Gen Hosp, Analyt & Translat Genet Unit, Boston, MA 02114 USA; 9.Univ Montreal, Dept Med, Montreal, PQ H1T 1C8, Canada; 10.MIT, Ctr Microbiome Informat & Therapeut, 77 Massachusetts Ave, Cambridge, MA 02139 USA |
推荐引用方式 GB/T 7714 | Mohanan, Vishnu,Nakata, Toru,Desch, A. Nicole,et al. C1orf106 is a colitis risk gene that regulates stability of epithelial adherens junctions[J]. SCIENCE,2018,359(6380):1161-+. |
APA | Mohanan, Vishnu.,Nakata, Toru.,Desch, A. Nicole.,Levesque, Chloe.,Boroughs, Angela.,...&Xavier, Ramnik J..(2018).C1orf106 is a colitis risk gene that regulates stability of epithelial adherens junctions.SCIENCE,359(6380),1161-+. |
MLA | Mohanan, Vishnu,et al."C1orf106 is a colitis risk gene that regulates stability of epithelial adherens junctions".SCIENCE 359.6380(2018):1161-+. |
条目包含的文件 | 条目无相关文件。 |
除非特别说明,本系统中所有内容都受版权保护,并保留所有权利。
修改评论