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Title:

From the Cover: CD39 deletion exacerbates experimental murine colitis and human polymorphisms increase susceptibility to inflammatory bowel disease.

Document type:
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Article
Author(s):
Friedman, DJ; Künzli, BM; A-Rahim, YI; Sévigny, J; Berberat, PO; Enjyoji, K; Csizmadia, E; Friess, H; Robson, SC
Abstract:
CD39/ENTPD1 hydrolyzes proinflammatory nucleotides to generate adenosine. As purinergic mediators have been implicated in intestinal inflammation, we hypothesized that CD39 might protect against inflammatory bowel disease. We studied these possibilities in a mouse model of colitis using mice with global CD39 deletion. We then tested whether human genetic polymorphisms in the CD39 gene might influence susceptibility to Crohn's disease. We induced colitis in mice using Dextran Sodium Sulfate (DSS)...     »
Journal title abbreviation:
Proc Natl Acad Sci U S A
Year:
2009
Journal volume:
106
Journal issue:
39
Pages contribution:
16788-93
Language:
eng
Fulltext / DOI:
doi:10.1073/pnas.0902869106
Pubmed ID:
http://view.ncbi.nlm.nih.gov/pubmed/19805374
Print-ISSN:
0027-8424
TUM Institution:
Chirurgische Klinik und Poliklinik
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