Gi2α protein deficiency: A model for inflammatory bowel disease View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

1995-11

AUTHORS

Uwe Rudolph, Milton J. Finegold, Susan S. Rich, Gregory R. Harriman, Yogambal Srinivasan, Philippe Brabet, Allan Bradley, LUTZ Birnbaumer

ABSTRACT

Mice deficient for the G protein subunit Gi2α were obtained by gene targeting. They displayed a growth retardation that was apparent at 6 weeks of age. They subsequently developed diffuse colitis with clinical and histopathological features closely resembling those of ulcerative colitis in humans. Seven of 20 Gi2α-deficient mice with colitis also developed adenocarcinomas of the colon. Gi2α-deficient thymocytes displayed two-to fourfold increases in mature CD4+8− and CD4−8+ phenotypes, an approximately threefold increase in highintensity CD3 staining and enhanced proliferative responses to T-cell receptor stimuli. Stimulation of Gi2α-deficient peripheral T cells induced a hyperresponsive profile of interleukin-2, tumor necrosis factor, and interferon-γ production, which may reflect a heightened response of primed cells or a defective negative regulation. We suggest that Gi2α-deficient mice may represent a useful animal model for dissecting the pathomechanisms of inflammatory bowel disease and also for the development of novel therapeutic strategies. More... »

PAGES

s101-s105

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/bf01540899

DOI

http://dx.doi.org/10.1007/bf01540899

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1050225627

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/8613481


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