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Ycf1p attenuates basal level oxidative stress response in Saccharomyces cerevisiae
Author(s) -
Paumi Christian M.,
Pickin Kerry A.,
Jarrar Roaa,
Herren Catherine K.,
Cowley Stuart T.
Publication year - 2012
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2012.02.010
Subject(s) - glutathione , oxidative stress , saccharomyces cerevisiae , phosphorylation , basal (medicine) , microbiology and biotechnology , chemistry , oxidative phosphorylation , salt (chemistry) , biochemistry , cellular stress response , function (biology) , biophysics , biology , fight or flight response , endocrinology , yeast , enzyme , gene , insulin
Ycf1p function is regulated by casein kinase 2 α , 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.