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

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 journal › Article › peer-review

Abstract

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 language	English (US)
Pages (from-to)	187-192
Number of pages	6
Journal	Receptors and Channels
Volume	5
Issue number	3-4
State	Published - 1997
Externally published	Yes

Keywords

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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abstract = "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.",

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T1 - Inactivation of the Gα(i2) and Gα(o) genes by homologous recombination

AU - Jiang, Meisheng

AU - Boulay, Guylain

AU - Spicher, Karsten

AU - Peyton, Michael J.

AU - Brabet, Philippe

AU - Birnbaumer, Lutz

AU - Rudolph, Uwe

PY - 1997

Y1 - 1997

N2 - 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.

AB - 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.

KW - Adenocarcinoma of the colon

KW - Binding regulatory protein

KW - Gene targeting

KW - Guanine nucleotide

KW - Ulcerative colitis

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SN - 1060-6823

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IS - 3-4

ER -

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

Abstract

Keywords

ASJC Scopus subject areas

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