The ARF-B23 Connection: Implications for Growth Control and Cancer Treatment
The ARF-B23 Connection: Implications for Growth Control and Cancer Treatment
复制标题
DOI：
10.4161/cc.3.3.719
复制
发表时间：
2004-03
期刊：
影响因子：
4.3
通讯作者：
Yanping Zhang
中科院分区：
文献类型：
--
作者：
Yanping Zhang
肿瘤抑制因子ARF诱导p53依赖性和非依赖性细胞周期阻滞。与核质定位的MDM2和p53不同，ARF定位于核仁。关于ARF在核仁中的作用以及其不依赖于p53的功能的分子靶点和机制仍然是一个有争议的研究领域。最近的研究发现核仁蛋白B23是ARF实现其生长抑制功能的靶点。ARF通过MDM2-p53途径阻断细胞周期进程并通过B23抑制核糖体生物发生的能力表明，ARF在协调抑制生长和增殖方面发挥作用。
The tumor suppressor ARF induces a p53-dependent and -independent cell cycle arrest. Unlike nucleoplasmic localized MDM2 and p53, ARF localizes in the nucleolus. The role of ARF in the nucleolus and the molecular target and mechanism of ARF’s p53-independent function remain both controversial and a fertile field of research. Recent study has identified the nucleolar protein B23 as a target of ARF for implementing its growth inhibitory function. The ability of ARF to block cell cycle progression through the MDM2-p53 pathway and to suppress ribosomal biogenesis through B23 suggest a role for ARF in coordinating inhibitions of growth and proliferation.