生物
倍性
钥匙(锁)
细胞生物学
河马信号通路
G2-M DNA损伤检查点
丝氨酸苏氨酸激酶
遗传学
计算生物学
细胞周期检查点
信号转导
细胞周期
癌症
磷酸化
基因
生态学
蛋白激酶A
作者
Bin Zhao,Kun‐Liang Guan
出处
期刊:Cell
[Cell Press]
日期:2014-08-01
卷期号:158 (4): 695-696
被引量:3
标识
DOI:10.1016/j.cell.2014.07.041
摘要
Tetraploid cells generated by abnormal cell division are often arrested during the cell cycle or cleared by apoptosis. Evasion of these defense mechanisms leads to genomic instability and tumorigenesis. In this issue, Ganem et al. report that extra centrosome-induced activation of the Hippo pathway kinase LATS2 is a key mechanism of tetraploidy-induced cell-cycle arrest.
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