论文部分内容阅读
基因组卫士p53在DNA损伤时能够迅速诱导细胞周期停滞和凋亡,从而防止肿瘤形成。最近这一观点受到挑战,Evan和Serrano等研究表明,DNA损伤的早期反应并非必需的,癌基因介导的p19ARF激活进而激活p53才是抑制肿瘤的关键环节。p53野生型小鼠经γ线照射后在敏感组织出现广泛的p53介导
Genome Guard p53 rapidly induces cell cycle arrest and apoptosis during DNA damage and thus prevents tumor formation. This view has been challenged recently, and studies by Evan and Serrano show that early response to DNA damage is not necessary. Oncogene-mediated activation of p19ARF and activation of p53 are key components of tumor suppression. p53 wild-type mice show extensive p53-mediated activation in sensitive tissues after gamma irradiation