Department of Toxicology, University of Kentucky, Lexington, KY 40536, USA.
FEBS Lett. 2012 Mar 23;586(6):847-53. doi: 10.1016/j.febslet.2012.02.010. Epub 2012 Feb 23.
Ycf1p function is regulated by casein kinase 2α, Cka1p, via phosphorylation of Ser251. Cka1p-mediated phosphorylation of Ycf1p is attenuated in response to high salt stress. Previous results from our lab suggest a role for Ycf1p in cellular resistance to salt stress. Here, we show that Ycf1p plays an important role in cellular resistance to salt stress by maintaining the cellular redox balance via glutathione recycling. Our results suggest that during acute salt stress increased Sod1p, Sod2p and Ctt1p activity is the main compensatory for the loss in Ycf1p function that results from reduced Ycf1p-dependent recycling of cellular GSH levels.
Ycf1p 的功能受酪蛋白激酶 2α(Cka1p)调控,通过 Ser251 丝氨酸磷酸化实现。Ycf1p 的 Cka1p 介导的磷酸化在高盐应激下受到抑制。我们实验室之前的研究结果表明 Ycf1p 在细胞对盐胁迫的抗性中发挥作用。在这里,我们通过谷胱甘肽循环证明 Ycf1p 通过维持细胞内氧化还原平衡在细胞对盐胁迫的抗性中发挥重要作用。我们的结果表明,在急性盐胁迫下, Sod1p、 Sod2p 和 Ctt1p 活性的增加是对 Ycf1p 功能丧失的主要补偿,这是由于 Ycf1p 依赖性细胞内 GSH 水平循环减少所致。