DNA damage tumor suppressor genes and genomic instability
摘要：
Disruption of the mechanisms that regulate cell-cycle checkpoints, DNA repair, and apoptosis results in genomic instability and the development of cancer in multicellular organisms. The protein kinases ATM and ATR, as well as their downstream substrates Chk1 and Chk2, are central players in checkpoint activation in response to DNA damage. Histone H2AX, ATRIP, as well as the BRCT-motif-containing molecules 53BP1, MDC1, and BRCA1 function as molecular adapters or mediators in the recruitment of ATM or ATR and their targets to sites of DNA damage. The increased chromosomal instability and tumor susceptibility apparent in mutant mice deficient in both p53 and either histone H2AX or proteins that contribute to the nonhomologous end-joining mechanism of DNA repair indicate that DNA damage checkpoints play a pivotal role in tumor suppression.
展开
DOI：
10.1016/j.gde.2003.12.003
被引量：
年份：
2004
通过文献互助平台发起求助，成功后即可免费获取论文全文。
相似文献
参考文献
引证文献
引用走势
站内活动
辅助模式
引用
文献可以批量引用啦~
欢迎点我试用！
