在 DNA 损伤和细胞衰老中，从 pRb/p105 向 Rb2/p130 的转变。
The switch from pRb/p105 to Rb2/p130 in DNA damage and cellular senescence.
机构信息
Department of Tumorvirology, Heinrich-Pette-Institute, Leibniz-Institute for Experimental Virology, Hamburg, Germany.
出版信息
J Cell Physiol. 2012 Feb;227(2):508-13. doi: 10.1002/jcp.22786.
PMID:21465484
Abstract
Cellular senescence is a response to genotoxic stress that results in an irreversible cell cycle arrest. Activation of this pathway relies on the activity of the retinoblastoma proteins and proteins of the DNA damage response cascade. Here, we discuss the functional relevance of the switch from pRb/p105 to Rb2/p130 that becomes apparent when cells enter senescent arrest.
摘要
细胞衰老（cellular senescence）是对遗传毒性应激的一种反应，导致细胞周期不可逆停滞。该途径的激活依赖于视网膜母细胞瘤蛋白（retinoblastoma proteins）和 DNA 损伤反应级联中的蛋白质的活性。在这里，我们讨论了细胞进入衰老停滞时 pRb/p105 向 Rb2/p130 的转换的功能相关性。
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