期刊
CANCER CELL
卷 19, 期 3, 页码 299-300出版社
CELL PRESS
DOI: 10.1016/j.ccr.2011.03.001
关键词
-
资金
- NHLBI NIH HHS [R01 HL035440-24, R01 HL079650, R01 HL035440, R01 HL035440-25, R01 HL079650-05] Funding Source: Medline
In this issue of Cancer Cell, Finley and coworkers report that the genetic loss of the deacetylase SIRT3 leads to metabolic reprogramming toward glycolysis. This shift is mediated by an increase in cellular reactive oxygen species (ROS) generation that amplifies HIF-alpha stabilization and HIF-dependent gene expression, thereby driving the tumor phenotype.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据