Abstract:
:STAT3, a transcription factor involved in various physiological and pathological processes, is also present in mitochondria. Mitochondrial STAT3 regulates complex I activity and reactive oxygen species (ROS) production, yet the mechanisms governing its translocation to mitochondria remain poorly understood. In this study, we show that rotenone-induced ROS triggers the Ser727 phosphorylation of STAT3 and its increased mitochondrial localisation. Furthermore, we show that STAT3-depleted cells display increased ROS levels during rotenone treatment. Targeted expression in mitochondria of wild-type STAT3 - but not S727A mutant - lowers ROS levels, indicating the importance of Ser727 phosphorylation, both in rotenone-induced mitochondrial targeting and quenching of ROS levels. Together, our results demonstrate a novel STAT3-mediated feedback mechanism to maintain redox homeostasis during stress.
journal_name
FEBS Lettjournal_title
FEBS lettersauthors
Mohammed F,Gorla M,Bisoyi V,Tammineni P,Sepuri NBVdoi
10.1002/1873-3468.13741subject
Has Abstractpub_date
2020-05-01 00:00:00pages
1403-1412issue
9eissn
0014-5793issn
1873-3468journal_volume
594pub_type
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