Non-apoptotic role of BID in inflammation and innate immunity

Garabet Yeretssian, Ricardo G. Correa, Karine Doiron, Patrick Fitzgerald, Christopher P. Dillon, Douglas R. Green, John C. Reed and Maya Saleh ()
Additional contact information
Garabet Yeretssian: McGill University
Ricardo G. Correa: Sanford-Burnham Medical Research Institute
Karine Doiron: McGill University
Patrick Fitzgerald: St. Jude Children’s Research Hospital
Christopher P. Dillon: St. Jude Children’s Research Hospital
Douglas R. Green: St. Jude Children’s Research Hospital
John C. Reed: Sanford-Burnham Medical Research Institute
Maya Saleh: McGill University

Nature, 2011, vol. 474, issue 7349, 96-99

Abstract: Role for BID in immunity The proapoptotic BCL2 family protein BID has been found to modulate inflammation and innate immunity in intestinal epithelial cells, independently of its role in apoptosis. BID acts through NOD1 and NOD2, the cytosolic sensors for bacterial peptidoglycans. This work points to BID as a possible therapeutic target for immune-mediated inflammatory conditions such as inflammatory bowel disease.

Date: 2011
References: Add references at CitEc
Citations:

Downloads: (external link)
https://www.nature.com/articles/nature09982 Abstract (text/html)
Access to the full text of the articles in this series is restricted.

Related works:
This item may be available elsewhere in EconPapers: Search for items with the same title.

Export reference: BibTeX RIS (EndNote, ProCite, RefMan) HTML/Text

Persistent link: https://EconPapers.repec.org/RePEc:nat:nature:v:474:y:2011:i:7349:d:10.1038_nature09982

Ordering information: This journal article can be ordered from
https://www.nature.com/

DOI: 10.1038/nature09982

Access Statistics for this article

Nature is currently edited by Magdalena Skipper

More articles in Nature from Nature
Bibliographic data for series maintained by Sonal Shukla () and Springer Nature Abstracting and Indexing ().