Oxidation state governs structural transitions in peroxiredoxin II that correlate with cell cycle arrest and recovery

被引:109
作者
Phalen, Timothy J.
Weirather, Kelly
Deming, Paula B.
Anathy, Vikas
Howe, Alan K.
van der Vliet, Albert
Jonsson, Thomas J.
Poole, Leslie B.
Heintz, Nicholas H. [1 ]
机构
[1] Univ Vermont, Coll Med, Dept Pathol, Burlington, VT 05405 USA
[2] Univ Vermont, Coll Med, Dept Pharmacol, Burlington, VT 05405 USA
[3] Wake Forest Univ, Sch Med, Ctr Struct Biol, Winston Salem, NC 27157 USA
关键词
D O I
10.1083/jcb.200606005
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Inactivation of eukaryotic 2-Cys peroxiredoxins (Prxs) by hyperoxidation has been proposed to promote accumulation of hydrogen peroxide (H2O2) for redox-dependent signaling events. We examined the oxidation and oligomeric states of PrxI and -II in epithelial cells during mitogenic signaling and in response to fluxes of H2O2. During normal mitogenic signaling, hyperoxidation of PrxI and -II was not detected. In contrast, H2O2-dependent cell cycle arrest was correlated with hyperoxidation of PrxII, which resulted in quantitative recruitment of similar to 66- and similar to 140-kD PrxII complexes into large filamentous oligomers. Expression of cyclin D1 and cell proliferation did not resume until PrxII-SO2H was reduced and native PrxII complexes were regenerated. Ectopic expression of PrxI or -II increased Prx-SO2H levels in response to oxidant exposure and failed to protect cells from arrest. We propose a model in which Prxs function as peroxide dosimeters in subcellular processes that involve redox cycling, with hyperoxidation controlling structural transitions that alert cells of perturbations in peroxide homeostasis.
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收藏
页码:779 / 789
页数:11
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