C1orf106 is a colitis risk gene that regulates stability of epithelial adherens junctions-Reference-Cited by-同舟云学术

C1orf106 is a colitis risk gene that regulates stability of epithelial adherens junctions

Published:2018-03-09 Issue:6380 Volume:359 Page:1161-1166
ISSN:0036-8075
Container-title:Science
language:en
Short-container-title:Science

Author:

Mohanan Vishnu¹²^ORCID,Nakata Toru¹²^ORCID,Desch A. Nicole¹²^ORCID,Lévesque Chloé³,Boroughs Angela²^ORCID,Guzman Gaelen¹^ORCID,Cao Zhifang²^ORCID,Creasey Elizabeth²^ORCID,Yao Junmei²^ORCID,Boucher Gabrielle³,Charron Guy³,Bhan Atul K.⁴⁵,Schenone Monica¹^ORCID,Carr Steven A.¹^ORCID,Reinecker Hans–Christian⁵⁶,Daly Mark J.¹⁵⁷^ORCID,Rioux John D.³⁸^ORCID,Lassen Kara G.¹²^ORCID,Xavier Ramnik J.¹²⁵⁶⁹^ORCID

Affiliation:

1. The Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA.

2. Center for Computational and Integrative Biology, Massachusetts General Hospital, Boston, MA 02114, USA.

3. Montreal Heart Institute Research Center, Montreal, Quebec H1T 1C8, Canada.

4. Pathology Department, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114, USA.

5. Center for the Study of Inflammatory Bowel Disease, Massachusetts General Hospital, Boston, MA 02114, USA.

6. Gastrointestinal Unit, Massachusetts General Hospital, Boston, MA 02114, USA.

7. Analytic and Translational Genetics Unit, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114, USA.

8. Department of Medicine, Université de Montréal, Montreal, Quebec H1T 1C8, Canada.

9. Center for Microbiome Informatics and Therapeutics, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.

Abstract

Overcoming a barrier to IBD Inflammatory bowel disease (IBD) is a group of disorders linked to inflammation of the gastrointestinal tract. Colitis is a type of IBD that affects the inner lining of the colon and has been linked to a gene known as C1orf106 . Mohanan et al. found that C1orf106 encodes a protein that stabilizes the integrity of epithelial junctions and enhances barrier defense (see the Perspective by Citi). IBD-associated mutations in C1orf106 lead to greater cytohesin-1 protein levels, changes in E-cadherin localization, and enhanced susceptibility to intestinal pathogens. Modulation of C1orf106 may thus hold promise for treating colitis and other IBDs. Science , this issue p. 1161 ; see also p. 1097

Funder

National Institutes of Health

Crohn's and Colitis Foundation of America

Canada Foundation for Innovation

Leona M. and Harry B. Helmsley Charitable Trust

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

Reference28 articles.

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2. Altered permeability in inflammatory bowel disease: pathophysiology and clinical implications