表明小径的河马是在肝尺寸控制和 tumorigenesis 起关键作用的一个 evolutionarily 保存的发信号的模块。河马小径由在的核心 kinase 串联组成哺乳动物的象 Ste20 一样 kinases (Mst1/2,果蝇河马的 orthologs ) 并且他们的余因子萨尔瓦多(Sav1 ) 形成建筑群到 phosphorylate 并且激活大肿瘤 suppressor (Lats1/2 ) 。Lats1/2 kinases 接着 phosphorylate 并且与 PDZ 有约束力的主题(TAZ ) 禁止抄写激活剂,联系是的蛋白质(笨蛋) 和 transcriptional 激活剂,河马小径的二个主要下游的受动器。河马小径部件的损失导致异常肝肿大和 tumorigenesis,笨蛋在协调房间增长和 apoptosis 的规定并且起一个必要作用。这评论总结在肝新生和 tumorigenesis 发信号的河马的规定的当前的调查结果,集中河马小径的肿瘤 suppressor 部件的损失怎么导致肝癌症并且讨论调整它在肝 tumorigenesis 的下游的受动器笨蛋的表示和激活的分子的机制。
The Hippo signaling pathway is an evolutionarily conserved signaling module that plays critical roles in liver size control and tumorigenesis. The Hippo pathway consists of a core kinase cascade in which the mammalian Ste20-1ike kinases (Mst1/2, orthologs of Drosophila Hippo) and their cofac- tor Salvador (Sav1) form a complex to phosphorylate and activate the large tumor suppressor (Lats1/2). Lats1/2 kinases in turn phosphorylate and inhibit the transcription co-activators, the Yes-associated protein (YAP) and the transcriptional co-activator with PDZ-binding motif (TAZ), two major down- stream effectors of the Hippo pathway. Losses of the Hippo pathway components induce aberrant hepatomegaly and tumorigenesis, in which YAP coordinates regulation of cell proliferation and apoptosis and plays an essential role. This review summarizes the current findings of the regulation of Hippo signaling in liver regeneration and tumorigenesis, focusing on how the loss of tumor sup- pressor components of the Hippo pathway results in liver cancers and discussing the molecular me- chanisms that regulate the expression and activation of its downstream effector YAP in liver tumorigenesis.