激酶的表达持续活跃alpha-PAK揭示影响肌动蛋白和焦复合物。
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黄程度E, HY,厕所,陈XQ,董JM, T梁,Lim L
激酶的表达持续活跃alpha-PAK揭示影响肌动蛋白和焦复合物。
摩尔细胞杂志。1997年3月,17 (3):1129 - 43。
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9032240 (在PubMed]
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短暂快速脉冲刺激导致蛋白蛋白激酶(柏加斯)21的家庭似乎存在于所有生物Cdc42-like gtpase。在哺乳动物细胞中,柏加斯已经与增殖作用的激活蛋白激酶级联,但没有报道这些激酶在细胞骨架的影响。最近我们已经表明,果蝇PAK浓缩在胚胎上皮细胞发生的前沿背闭包(H.-Y n .硬化j . Lee。Loh, Y.-M。Ong Tan, t梁,大肠程度和l . Lim摩尔。细胞。生物16:1896 - 1908,1996),它与结构类似焦colocalizes复合物。我们这里显示上皮海拉细胞的转染,alpha-PAK从细胞质中招募到不同的焦复合物由Cdc42 (G12V)和Rac1 (G12V),自己colocalize这些网站。通过删除分析,显示了N末端PAK为焦粘连包含目标序列表明,这些复合物在体内激酶功能的网站。Cdc42 Rac1导致alpha-PAK自身磷酸化激酶激活。映射alpha-PAK自身磷酸化网站已允许代一个既定的活跃的激酶突变。 By fusing regions of Cdc42 to the C terminus of PAK, activated chimeras were also obtained. Plasmids encoding these different constitutively active alpha-PAKs caused loss of stress fibers when introduced into both HeLa cells and fibroblasts, which was similar to the effect of introducing Cdc42(G12V) or Rac1(G12V). Significantly dramatic losses of focal adhesions were also observed. These combined effects resulted in retraction of the cell periphery after plasmid microinjection. These data support our previous suggestions of a role for PAK downstream of both Cdc42 and Rac1 and indicate that PAK functions include the dissolution of stress fibers and reorganization of focal complexes.