Function of Mitochondrial Stat3 in Cellular Respiration-Reference-Cited by-同舟云学术

Function of Mitochondrial Stat3 in Cellular Respiration

Published:2009-02-06 Issue:5915 Volume:323 Page:793-797
ISSN:0036-8075
Container-title:Science
language:en
Short-container-title:Science

Author:

Wegrzyn Joanna¹²³⁴⁵,Potla Ramesh¹²³⁴⁵,Chwae Yong-Joon¹²³⁴⁵,Sepuri Naresh B. V.¹²³⁴⁵,Zhang Qifang¹²³⁴⁵,Koeck Thomas¹²³⁴⁵,Derecka Marta¹²³⁴⁵,Szczepanek Karol¹²³⁴⁵,Szelag Magdalena¹²³⁴⁵,Gornicka Agnieszka¹²³⁴⁵,Moh Akira¹²³⁴⁵,Moghaddas Shadi¹²³⁴⁵,Chen Qun¹²³⁴⁵,Bobbili Santha¹²³⁴⁵,Cichy Joanna¹²³⁴⁵,Dulak Jozef¹²³⁴⁵,Baker Darren P.¹²³⁴⁵,Wolfman Alan¹²³⁴⁵,Stuehr Dennis¹²³⁴⁵,Hassan Medhat O.¹²³⁴⁵,Fu Xin-Yuan¹²³⁴⁵,Avadhani Narayan¹²³⁴⁵,Drake Jennifer I.¹²³⁴⁵,Fawcett Paul¹²³⁴⁵,Lesnefsky Edward J.¹²³⁴⁵,Larner Andrew C.¹²³⁴⁵

Affiliation:

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

2. Department of Medical Biotechnology, Faculty of Biochemistry, Biophysics, and Biotechnology, Jagiellonian University, Krakow, Poland.

3. Department of Biology, Cleveland State University, Cleveland, OH 44114, USA.

4. Department of Biochemistry, School of Life Sciences, University of Hyderabad, Hyderabad 500 046, India.

5. Department of Pathobiology, Lerner Research Institute, The Cleveland Clinic Foundation, 9500 Euclid Avenue, Cleveland, OH 44195, USA.

Abstract

Cytokines such as interleukin-6 induce tyrosine and serine phosphorylation of Stat3 that results in activation of Stat3-responsive genes. We provide evidence that Stat3 is present in the mitochondria of cultured cells and primary tissues, including the liver and heart. In Stat3 â/â cells, the activities of complexes I and II of the electron transport chain (ETC) were significantly decreased. We identified Stat3 mutants that selectively restored the protein's function as a transcription factor or its functions within the ETC. In mice that do not express Stat3 in the heart, there were also selective defects in the activities of complexes I and II of the ETC. These data indicate that Stat3 is required for optimal function of the ETC, which may allow it to orchestrate responses to cellular homeostasis.

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

Reference17 articles.

1. Hematopoietic cytokine receptor signaling

2. Identification of GRIM-19, a Novel Cell Death-regulatory Gene Induced by the Interferon-β and Retinoic Acid Combination, Using a Genetic Approach

3. GRIM-19, a death-regulatory gene product, suppresses Stat3 activity via functional interaction

4. The cell death regulator GRIM-19 is an inhibitor of signal transducer and activator of transcription 3

5. GRIM-19, a Cell Death Regulatory Gene Product, Is a Subunit of Bovine Mitochondrial NADH:Ubiquinone Oxidoreductase (Complex I)

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