Jiang M, Boulay G, Spicher K, Peyton M J, Brabet P, Birnbaumer L, Rudolph U
Department of Anesthesiology, School of Medicine, University of California, Los Angeles 90095-1778, USA.
Recept Channels. 1997;5(3-4):187-92.
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.
G蛋白将受体与效应器偶联，从而调节多种生物学过程。在此，我们报告Gαi2缺陷型和Gαo缺陷型小鼠的表型。Gαi2缺陷型小鼠表现出对腺苷酸环化酶的抑制调节减弱、T细胞成熟和功能改变、生长迟缓，还会发展出一种致命的弥漫性结肠炎，其临床和组织病理学特征与人类溃疡性结肠炎极为相似，包括结肠癌的发生。Gαo缺陷型小鼠也能存活，但明显比野生型对照小鼠小。
