Oxidative stress activates AMPK in cultured cells primarily by increasing cellular AMP and/or ADP.
Oxidative stress activates AMPK in cultured cells primarily by increasing cellular AMP and/or ADP.
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DOI：
10.1016/j.febslet.2014.07.025
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发表时间：
2014-09-17
期刊：
影响因子：
3.5
通讯作者：
Hardie DG
中科院分区：
文献类型：
--
作者：
Auciello FR;Ross FA;Ikematsu N;Hardie DG
AMPK被葡萄糖氧化酶产生的氧化应激激活。激活在很大程度上但不是唯一地由AMP和/或ADP的增加介导。Thr 172磷酸化的增加是由去磷酸化的抑制介导的。已知AMPK被氧化应激激活。向细胞中添加葡萄糖氧化酶以恒定速率产生H2 O2，这与酶降解相反，为生理氧化应激提供了良好的模型。葡萄糖氧化酶对AMPK的激活与细胞AMP：ATP的增加相关，并且在表达AMP不敏感的AMPK突变体的细胞中大大减少，尽管仍保留了少量的激活。AMP增加的影响部分是由于抑制Thr 172去磷酸化。这些结果表明，腺嘌呤核苷酸的变化，而不是直接的氧化修饰，是氧化应激过程中AMPK激活的主要驱动因素。
AMPK is activated by oxidative stress generated using glucose oxidase. Activation is largely, but not solely, mediated by increases in AMP and/or ADP. Increases in Thr172 phosphorylation are mediated by inhibition of dephosphorylation. AMPK is known to be activated by oxidative stress. Addition of glucose oxidase to cells generates H2O2 at a constant rate that is opposed by enzymic degradation, providing a good model for physiological oxidative stress. AMPK activation by glucose oxidase correlated with increases in cellular AMP:ATP and was greatly reduced in cells expressing an AMP-insensitive AMPK mutant, although a small degree of activation remained. The effects of increased AMP were partly due to inhibition of Thr172 dephosphorylation. These results suggest that changes in adenine nucleotides, rather than direct oxidative modification, are the major drivers of AMPK activation during oxidative stress.
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影响因子：
--
作者：
Hawley SA;Boudeau J;Reid JL;Mustard KJ;Udd L;Mäkelä TP;Alessi DR;Hardie DG
通讯作者：
Hardie DG
影响因子：
29
作者：
Gowans GJ;Hawley SA;Ross FA;Hardie DG
通讯作者：
Hardie DG
影响因子：
7.7
作者：
Hardie DG
通讯作者：
Hardie DG
影响因子：
3.5
作者：
Davies, SP;Helps, NR;Hardie, DG
通讯作者：
Hardie, DG
影响因子：
9.2
作者：
Woods, A;Johnstone, SR;Carling, D
通讯作者：
Carling, D