Modulation of intracellular ROS levels by TIGAR controls autophagy.
Modulation of intracellular ROS levels by TIGAR controls autophagy.
复制标题
DOI：
10.1038/emboj.2009.242
复制
发表时间：
2009-10-07
期刊：
影响因子：
11.4
通讯作者：
Vousden, Karen H.
中科院分区：
文献类型：
--
作者：
Bensaad, Karim;Cheung, Eric C.;Vousden, Karen H.
p53诱导的Tigar蛋白作为果糖2,6-双磷酸酶的功能，促进五肽磷酸盐途径，并有助于降低细胞内反应性氧（ROS）的作用（ROS）。在这项研究中，诸如营养饥饿和代谢应激之类抑制自噬的功能。通过限制ROS水平的反应。与调节糖酵解的Tigar相似，可以通过ROS调节对自噬反应产生深远的影响。
The p53-inducible TIGAR protein functions as a fructose-2,6-bisphosphatase, promoting the pentose phosphate pathway and helping to lower intracellular reactive oxygen species (ROS). ROS functions in the regulation of many cellular responses, including autophagy—a response to stress conditions such as nutrient starvation and metabolic stress. In this study, we show that TIGAR can modulate ROS in response to nutrient starvation or metabolic stress, and functions to inhibit autophagy. The ability of TIGAR to limit autophagy correlates strongly with the suppression of ROS, with no clear effects on the mTOR pathway, and is p53 independent. The induction of autophagy in response to loss of TIGAR can function to moderate apoptotic response by restraining ROS levels. These results reveal a complex interplay in the regulation of ROS, autophagy and apoptosis in response to TIGAR expression, and shows that proteins similar to TIGAR that regulate glycolysis can have a profound effect on the autophagic response through ROS regulation.
登录
查看更多内容
影响因子：
13.3
作者：
Crighton, Diane;Wilkinson, Simon;Ryan, Kevin M.
通讯作者：
Ryan, Kevin M.
影响因子：
16
作者：
Jones, RG;Plas, DR;Thompson, CB
通讯作者：
Thompson, CB
影响因子：
11.2
作者：
Kopnin, Pavel B.;Agapova, Larissa S.;Chumakov, Peter M.
通讯作者：
Chumakov, Peter M.
影响因子：
12.4
作者：
Chen, Y.;McMillan-Ward, E.;Gibson, S. B.
通讯作者：
Gibson, S. B.
影响因子：
64.5
作者：
Colell, Anna;Ricci, Jean-Ehrland;Green, Douglas R.
通讯作者：
Green, Douglas R.