v-src介导的细胞转化需要Stat3激活。
Stat3 activation is required for cellular transformation by v-src.
作者信息
Bromberg J F, Horvath C M, Besser D, Lathem W W, Darnell J E
机构信息
Laboratory of Molecular Cell Biology, The Rockefeller University, New York, New York 10021-6399, USA.
出版信息
Mol Cell Biol. 1998 May;18(5):2553-8. doi: 10.1128/MCB.18.5.2553.
Abstract
Stat3 activation has been associated with cytokine-induced proliferation, anti-apoptosis, and transformation. Constitutively activated Stat3 has been found in many human tumors as well as v-abl- and v-src-transformed cell lines. Because of these correlations, we examined directly the relationship of activated Stat3 to cellular transformation and found that wild-type Stat3 enhances the transforming potential of v-src while three dominant negative Stat3 mutants inhibit v-src transformation. Stat3 wild-type or mutant proteins did not affect v-ras transformation. We conclude that Stat3 has a necessary role in v-src transformation.
摘要
Stat3激活与细胞因子诱导的增殖、抗凋亡及转化相关。在许多人类肿瘤以及v-abl和v-src转化的细胞系中均发现有组成型激活的Stat3。基于这些相关性，我们直接检测了激活的Stat3与细胞转化之间的关系，发现野生型Stat3增强了v-src的转化潜能，而三个显性负性Stat3突变体抑制了v-src转化。Stat3野生型或突变型蛋白不影响v-ras转化。我们得出结论，Stat3在v-src转化中起必要作用。
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