p66（Shc）基因在人类细胞系中具有促凋亡作用，且它是通过一条不依赖p53的途径被激活的。
p66(Shc) gene has a pro-apoptotic role in human cell lines and it is activated by a p53-independent pathway.
作者信息
Tiberi Luca, Faisal Amir, Rossi Matteo, Di Tella Lucia, Franceschi Claudio, Salvioli Stefano
机构信息
Department of Experimental Pathology, University of Bologna, via S. Giacomo 12, 40126 Bologna, Italy.
出版信息
Biochem Biophys Res Commun. 2006 Apr 7;342(2):503-8. doi: 10.1016/j.bbrc.2006.02.007. Epub 2006 Feb 9.
p66(Shc) protein has been proposed to be an indispensable factor for p53-dependent, mitochondria-mediated apoptosis in mice. Here, we show that p66(Shc) plays a pro-apoptotic role also in cell lines of human origin such as SaOs-2 and HeLa, where p53 is either absent or inactivated, thus, suggesting that p66(Shc) pro-apoptotic role is independent from the presence of a functional form of p53. The active form of p66(Shc) is phosphorylated in Serine 36. We confirm the importance of Serine 36 phosphorylation for p66(Shc) pro-apoptotic role, and our results suggest that the kinase involved in this process is activated independently from p53.
p66（Shc）蛋白被认为是小鼠中p53依赖性、线粒体介导的细胞凋亡所必需的因子。在此，我们表明p66（Shc）在人源细胞系如SaOs-2和HeLa中也发挥促凋亡作用，在这些细胞系中p53要么缺失要么失活，因此，这表明p66（Shc）的促凋亡作用独立于功能性p53的存在。p66（Shc）的活性形式在丝氨酸36处被磷酸化。我们证实了丝氨酸36磷酸化对于p66（Shc）促凋亡作用的重要性，并且我们的结果表明参与此过程的激酶独立于p53被激活。
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