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Angiomotin’g YAP into the Nucleus for Cell Proliferation and Cancer Development
Wanjin Hong ; Hong WJ(洪万进)
2013-09-03
英文摘要文章阐述了Hippo信号通路下游蛋白YAP新的调节机制。Hippo信号通路通过调节细胞增殖和凋亡,可调节器官大小以及肿瘤发生等重要功能,而转录因子辅助因子YAP(Yes-Associated Protein)是这一信号通路中的一个关键蛋白,该蛋白需转运到细胞核内才能发挥其致癌作用。传统观点认为YAP的调节蛋白——Angiomotin (Amot)可通过与YAP的结合,使其滞留在细胞质内以便被蛋白酶降解,因而认为Amot 是抑癌基因。洪教授对Yi,CL 等在同期Science Signaling发表的有关Amot通过蛋白-蛋白之间的相互作用而促进 YAP向细胞核转运的成果进行了评述,并提出了Amot调控YAP的新模型,该模型的提出为肿瘤的综合治疗提供了新思路,具有重要的理论和实践意义。; The Hippo pathway regulates cell proliferation and apoptosis during development, tissue regeneration, and carcinogenesis. Nuclear translocation of the transcription factors Yes-associated protein (YAP) and transcriptional coactivator with PDZ-binding motif (TAZ) and their subsequent interaction with TEA domain (TEAD) transcriptional factors program pro-proliferative and antiapoptotic transcription. Scaffold proteins angiomotin (Amot) and angiomotin-related AmotL1 and AmotL2 were recently identified as negative regulators of YAP and TAZ by preventing their nuclear translocation. In this issue of Science Signaling, Yi et al. show that Amot may also promote nuclear translocation of YAP and act as a transcriptional cofactor of the YAP-TEAD complex to facilitate proliferation of biliary epithelial cells and cancer development of the liver either in response to tissue injury or in the absence of the tumor suppressor Merlin. These seemingly controversial results highlight that our understanding of Amot proteins in the Hippo pathway is so far limited.; http://news.xmu.edu.cn/s/13/t/542/22/40/info139840.htm
语种英语
出版者American Association for the Advancement of Science
内容类型期刊论文
源URL[http://dx.doi.org/10.1126/scisignal.2004573]  
专题药学院-已发表论文
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GB/T 7714
Wanjin Hong,Hong WJ. Angiomotin’g YAP into the Nucleus for Cell Proliferation and Cancer Development[J],2013.
APA Wanjin Hong,&洪万进.(2013).Angiomotin’g YAP into the Nucleus for Cell Proliferation and Cancer Development..
MLA Wanjin Hong,et al."Angiomotin’g YAP into the Nucleus for Cell Proliferation and Cancer Development".(2013).
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