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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Inactivation of the G alpha i2 and G alpha o genes by homologous recombination.

G proteins couple receptors to effectors and thus regulate multiple biological processes. Here we report on the phenotypes of G alpha i2-deficient and G alpha o-deficient mice. G alpha i2-deficient mice display a blunted inhibitory regulation of adenylyl cyclase, alterations in T cell maturation and function, a growth retardation and also develop a lethal diffuse colitis with clinical and histopathological features closely resembling ulcerative colitis in humans, including the development of adenocarcinoma of the colon. G alpha o-deficient mice are also viable, but significantly smaller than wild-type controls.[1]


  1. Inactivation of the G alpha i2 and G alpha o genes by homologous recombination. Jiang, M., Boulay, G., Spicher, K., Peyton, M.J., Brabet, P., Birnbaumer, L., Rudolph, U. Recept. Channels (1997) [Pubmed]
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