Kohn A D, Barthel A, Kovacina K S, Boge A, Wallach B, Summers S A, Birnbaum M J, Scott P H, Lawrence J C, Roth R A
Department of Molecular Pharmacology, Stanford University School of Medicine, Stanford, California 94305, USA.
J Biol Chem. 1998 May 8;273(19):11937-43. doi: 10.1074/jbc.273.19.11937.
Akt is a serine/threonine kinase that requires a functional phosphatidylinositol 3-kinase to be stimulated by insulin and other growth factors. When directed to membranes by the addition of a src myristoylation sequence, Akt becomes constitutively active. In the present study, a conditionally active version of Akt was constructed by fusing the Akt containing the myristoylation sequence to the hormone binding domain of a mutant murine estrogen receptor that selectively binds 4-hydroxytamoxifen. The chimeric protein was expressed in NIH3T3 cells and was shown to be stimulated by hormone treatment 17-fold after only a 20-min treatment. This hormone treatment also stimulated an approximate 3-fold increase in the phosphorylation of the chimeric protein and a shift in its migration on SDS gels. Activation of this conditionally active Akt resulted in the rapid stimulation of the 70-kDa S6 kinase. This conditionally active Akt was also found to rapidly stimulate in these cells the phosphorylation of properties of PHAS-I, a key protein in the regulation of protein synthesis. The conditionally active Akt, when expressed in 3T3-L1 adipocytes, was also stimulated, although its rate and extent of activation was less then in the NIH3T3 cells. Its stimulation was shown to be capable of inducing glucose uptake into adipocytes by stimulating translocation of the insulin-responsive glucose transporter GLUT4 to the plasma membrane.
Akt是一种丝氨酸/苏氨酸激酶,需要功能性磷脂酰肌醇3激酶才能被胰岛素和其他生长因子激活。当通过添加src肉豆蔻酰化序列将其导向细胞膜时,Akt会持续激活。在本研究中,通过将含有肉豆蔻酰化序列的Akt与选择性结合4-羟基他莫昔芬的突变小鼠雌激素受体的激素结合域融合,构建了一种条件性激活的Akt。嵌合蛋白在NIH3T3细胞中表达,经20分钟激素处理后,其活性被激素刺激增强了17倍。这种激素处理还使嵌合蛋白的磷酸化增加了约3倍,并使其在SDS凝胶上的迁移发生改变。激活这种条件性激活的Akt导致70 kDa S6激酶迅速被激活。还发现这种条件性激活的Akt能在这些细胞中迅速刺激PHAS-I(蛋白质合成调控中的关键蛋白)的磷酸化。当在3T3-L1脂肪细胞中表达时,条件性激活的Akt也被激活,尽管其激活速率和程度低于在NIH3T3细胞中的情况。其激活被证明能够通过刺激胰岛素反应性葡萄糖转运蛋白GLUT4向质膜的转位来诱导葡萄糖摄取到脂肪细胞中。