蛋白激酶B
磷酸化
激酶
细胞生物学
MAP激酶激酶激酶
地图2K7
蛋白激酶A
丝裂原活化蛋白激酶激酶
化学
细胞周期蛋白依赖激酶2
癌症研究
生物
作者
Luis del Peso,Maribel González-Garcı́a,Carmen Page,Román Herrera,Gabriel Núñez
出处
期刊:Science
[American Association for the Advancement of Science (AAAS)]
日期:1997-10-24
卷期号:278 (5338): 687-689
被引量:2218
标识
DOI:10.1126/science.278.5338.687
摘要
BAD is a distant member of the Bcl-2 family that promotes cell death. Phosphorylation of BAD prevents this. BAD phosphorylation induced by interleukin-3 (IL-3) was inhibited by specific inhibitors of phosphoinositide 3-kinase (PI 3-kinase). Akt, a survival-promoting serine-threonine protein kinase, was activated by IL-3 in a PI 3-kinase–dependent manner. Active, but not inactive, forms of Akt were found to phosphorylate BAD in vivo and in vitro at the same residues that are phosphorylated in response to IL-3. Thus, the proapoptotic function of BAD is regulated by the PI 3-kinase–Akt pathway.
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