Stress-induced dynamic regulation of mitochondrial STAT3 and its association with cyclophilin D reduce mitochondrial ROS production

Author:

Meier Jeremy A.12ORCID,Hyun Moonjung2ORCID,Cantwell Marc12,Raza Ali23ORCID,Mertens Claudia4,Raje Vidisha2ORCID,Sisler Jennifer2,Tracy Erin5ORCID,Torres-Odio Sylvia6,Gispert Suzana6,Shaw Peter E.7,Baumann Heinz5,Bandyopadhyay Dipankar8,Takabe Kazuaki23910ORCID,Larner Andrew C.2ORCID

Affiliation:

1. Center for Clinical and Translational Research, Virginia Commonwealth University, Richmond, VA 23298, USA.

2. Department of Biochemistry and Molecular Biology and Massey Cancer Center, Virginia Commonwealth University, Richmond, VA 23298, USA.

3. Division of Surgical Oncology, Virginia Commonwealth University School of Medicine, Richmond, VA 23298, USA.

4. Laboratory of Molecular Cell Biology, Rockefeller University, New York, NY 10065, USA.

5. Department of Molecular and Cellular Biology, Roswell Park Cancer Institute, Buffalo, NY 14263, USA.

6. Experimental Neurology, Goethe University Medical School, Frankfurt am Main, Germany.

7. School of Life Sciences, University of Nottingham, Nottingham, U.K.

8. Department of Biostatistics, Virginia Commonwealth University School of Medicine, Richmond, VA 23298, USA.

9. Division of Breast Surgery, Department of Surgical Oncology, Roswell Park Cancer Institute, Buffalo, NY 14263, USA.

10. Department of Surgery, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, Buffalo, NY 14203, USA.

Abstract

Stress depletes STAT3 in the mitochondria, and restoration of this STAT3 pool suppresses stress-induced ROS production.

Funder

National Cancer Institute

National Institute of General Medical Sciences

National Center for Advancing Translational Sciences

British Heart Foundation

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Cell Biology,Molecular Biology,Biochemistry

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