Inactivation of the Gα(i2) and Gα(o) genes by homologous recombination

Meisheng Jiang, Guylain Boulay, Karsten Spicher, Michael J. Peyton, Philippe Brabet, Lutz Birnbaumer, Uwe Rudolph

Research output: Contribution to journalArticlepeer-review


G proteins couple receptors to effectors and thus regulate multiple biological processes. Here we report on the phenotypes of Gα(i2)-deficient and Gα(o)-deficient mice. Ga(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. Gα(o)-deficient mice are also viable, but significantly smaller than wild-type controls.

Original languageEnglish (US)
Pages (from-to)187-192
Number of pages6
JournalReceptors and Channels
Issue number3-4
StatePublished - 1997
Externally publishedYes


  • Adenocarcinoma of the colon
  • Binding regulatory protein
  • Gene targeting
  • Guanine nucleotide
  • Ulcerative colitis

ASJC Scopus subject areas

  • Pharmacology
  • Endocrinology
  • Clinical Biochemistry
  • Cell Biology


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