Carrascosa J M, Vogt B, Ullrich A, Häring H U
Institut für Diabetesforschung, München, Germany.
Biochem Biophys Res Commun. 1991 Jan 15;174(1):123-7. doi: 10.1016/0006-291x(91)90494-r.
Activation of a phosphatidylinositol-3-kinase (PI-3-kinase) is one of the earliest consequences of insulin binding to the receptor. The human insulin receptor exists in two isoforms which differ in the length of the alpha-subunit (HIR-A = 719 aa, HIR-B = 731 aa). To test whether both isoforms transduce an insulin signal on PI-3-kinase we used rat-1-fibroblasts expressing HIR-A or HIR-B. We found that insulin stimulates 32P incorporation into PIP through both HIR-A and HIR-B to a similar extent (approx. 8-10 fold).
磷脂酰肌醇-3-激酶(PI-3-激酶)的激活是胰岛素与受体结合最早产生的结果之一。人胰岛素受体存在两种亚型,其α亚基长度不同(HIR-A = 719个氨基酸,HIR-B = 731个氨基酸)。为了检测这两种亚型是否都能在PI-3-激酶上转导胰岛素信号,我们使用了表达HIR-A或HIR-B的大鼠-1成纤维细胞。我们发现胰岛素通过HIR-A和HIR-B刺激32P掺入PIP的程度相似(约8-10倍)。