ALK 信号通路诱导的核事件
中文名称
通路描述
通过致癌形式的 ALK 信号激活核事件，驱动细胞生存、逃避凋亡和转化（综述：Della Corte 等，2018；Roskoski，2013；Chiarle 等，2008）。基因表达的变化既由表观遗传机制介导，也由诱导关键转录因子和细胞周期调节因子的表达所实现，以及其他关键靶点。许多这些基因表达事件依赖于 STAT3 的激活，以及 ALK 下游的 MAP 激酶信号（综述：Hallberg 和 Palmer，2013；Hallberg 和 Palmer，2016；Ducray 等，2019）。与迄今为止鉴定出的融合蛋白相比，已研究的 NPM-ALK 融合蛋白似乎由于与内源性全长 NPM 的寡聚化而部分定位于细胞核中。
英文描述
Nuclear events stimulated by ALK signaling in cancer Signaling through oncogenic forms of ALK activate nuclear events that drive cellular survival, escape from apoptosis and transformation (reviewed in Della Corte et al, 2018; Roskoski, 2013; Chiarle et al, 2008). Changes to gene expression are effected both by epigenetic mechanisms and by inducing expression of key transcription factors and cell cycle regulators, among other critical targets. Many of these gene expression events are dependent on activation of STAT3 and to a lesser extent, MAP kinase signaling downstream of ALK (reviewed in Hallberg and Palmer, 2013; Hallberg and Palmer, 2016; Ducray et al, 2019). Unique among fusion proteins identified to date, the well-studied NPM-ALK fusion appears to be partially localized to the nucleus by virtue of oligomerization with endogenous full-length NPM.
所含基因
33 个基因