| Literature DB >> 19131594 |
Joanna Wegrzyn1, Ramesh Potla, Yong-Joon Chwae, Naresh B V Sepuri, Qifang Zhang, Thomas Koeck, Marta Derecka, Karol Szczepanek, Magdalena Szelag, Agnieszka Gornicka, Akira Moh, Shadi Moghaddas, Qun Chen, Santha Bobbili, Joanna Cichy, Jozef Dulak, Darren P Baker, Alan Wolfman, Dennis Stuehr, Medhat O Hassan, Xin-Yuan Fu, Narayan Avadhani, Jennifer I Drake, Paul Fawcett, Edward J Lesnefsky, Andrew C Larner.
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(-/-) 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.Entities:
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Year: 2009 PMID： 19131594 PMCID： PMC2758306 DOI： 10.1126/science.1164551
Source DB: PubMed Journal: Science ISSN： 0036-8075 Impact factor: 47.728