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.
Jiang
M
M
Department of Anesthesiology, School of Medicine, University of California, Los Angeles 90095-1778, USA.
Boulay
G
G
Spicher
K
K
Peyton
M J
MJ
Brabet
P
P
Birnbaumer
L
L
Rudolph
U
U
D000818:Animals; D051960:GTP-Binding Protein alpha Subunit, Gi2; D019206:GTP-Binding Protein alpha Subunits, Gi-Go; D019204:GTP-Binding Proteins / Q000235:genetics / Q000502:physiology*; D017353:Gene Deletion; D051379:Mice; D018345:Mice, Knockout; D011518:Proto-Oncogene Proteins / Q000235:genetics / Q000502:physiology*; D011995:Recombination, Genetic
D011518:Proto-Oncogene Proteins; D019204:GTP-Binding Proteins; D051960:GTP-Binding Protein alpha Subunit, Gi2; D019206:GTP-Binding Protein alpha Subunits, Gi-Go; C498016:Gnai2 protein, mouse