Circadian Oscillation of Sulfiredoxin in the Mitochondria
作者： In Sup Kil , Keun Woo Ryu , Se Kyoung Lee , Jeong Yeon Kim , Sei Yoon Chu
DOI: 10.1016/J.MOLCEL.2015.06.031
关键词: Biology 、 Heat shock protein 、 Peroxiredoxin III 、 Cytosol 、 Transport protein 、 Sulfiredoxin 、 Cell biology 、 Proteolysis 、 Mitochondrion 、 Oscillation (cell signaling)
摘要: Hydrogen peroxide (H2O2) released from mitochondria regulates various cell signaling pathways. Given that H2O2-eliminating enzymes such as peroxiredoxin III (PrxIII) are abundant in mitochondria, however, it has remained unknown how release can occur. Active PrxIII-SH undergoes reversible inactivation via hyperoxidation to PrxIII-SO2, which is then reduced by sulfiredoxin. We now show the amounts of PrxIII-SO2 and sulfiredoxin undergo antiphasic circadian oscillation specific tissues mice maintained under normal conditions. Cytosolic was found be imported into a mechanism requires formation disulfide-linked complex with heat shock protein 90, promoted H2O2 mitochondria. The degraded Lon manner dependent on PrxIII state. coordinated import degradation provide basis for consequent likely result an oscillatory release.
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