AKT1 E17K 在癌症中的持续信号传导
中文名称
通路描述
虽然癌症中 AKT1 基因拷贝数、表达水平和磷酸化水平通常增加，但仅有一种低频点突变被反复报道并进行了功能研究。该突变代表 AKT1 第 17 位谷氨酸残基被赖氨酸取代，并通过使 AKT1 结合 PIP2 发挥作用。PIP2 结合的 AKT1 由 TORC2 复合物和始终存在于细胞膜上的 PDPK1 磷酸化，这是由于 PIP2 亲和力低所致。因此，E17K 取代消除了 AKT1 激活所需的 PI3K（Carpten et al. 2007, Landgraf et al. 2008）。
英文描述
STAT6-mediated induction of chemokines Signal transducer and activator of transcription 6 (STAT6) may function as a signaling molecule and as a transcription factor. The canonical activation of STAT6 in IL4 and IL13 signaling pathways is mediated by the tyrosine kinases JAK (Hebenstreit D et al. 2006). Virus-induced STAT6 activation was found to be cytokine- and JAK-independent (Chen H et al. 2011). Infection of human cells with RNA or DNA viruses resulted in an interaction of STAT6 with STING. The kinase TBK1 was shown to phosphorylate STAT6, which in turn induced STAT6 dimerization and translocation to the nucleus, leading to induction of chemokines CCL2, CCL20, and CCL26 in IFN-independent manner (Chen H et al. 2011).RNA virus infection triggers STAT6 activation through STING, TBK1 and adaptor protein MAVS interaction (Chen H et al. 2011).
所含基因
3 个基因