Pluquet O, Hainaut P
Group of Molecular Carcinogenesis, International Agency for Research on Cancer, 150 Cours Albert Thomas, 69372, Lyon, France.
Cancer Lett. 2001 Dec 10;174(1):1-15. doi: 10.1016/s0304-3835(01)00698-x.
Since the initial concept of p53 as a sensor of DNA-damage, the picture of the role of p53 has widened to include the sensing of much more diverse forms of stress, including hypoxia and constitutive activation of growth-promoting cascades. The pathways by which these processes regulate p53 are partially overlapping, but imply different patterns of post-translational modifications. In this review, we summarize current knowledge on post-translational modifications of p53, and we discuss how hypoxia and oncogene activation stresses may induce p53 independently of DNA damage.
自从p53最初被视为DNA损伤的传感器以来，p53作用的范畴已得到扩展，涵盖了对更多种不同形式应激的感知，包括缺氧以及促进生长级联反应的组成型激活。这些过程调节p53的途径部分重叠，但意味着不同的翻译后修饰模式。在本综述中，我们总结了关于p53翻译后修饰的当前知识，并讨论了缺氧和癌基因激活应激如何在不依赖DNA损伤的情况下诱导p53。
