Note to users. If you're seeing this message, it means that your browser cannot find this page's style/presentation instructions -- or possibly that you are using a browser that does not support current Web standards. Find out more about why this message is appearing, and what you can do to make your experience of our site the best it can be.
Sci. Signal., 29 September 2009
Vol. 2, Issue 90, p. pe61
STAT3 Revs Up the Powerhouse
Nancy C. Reich*
Molecular Genetics and Microbiology, Stony Brook University, Stony Brook, NY 11794, USA.
Tyrosine phosphorylation of signal transducers and activators of transcription (STATs) promotes their dimerization and ability to bind target genes in the nucleus. However, evidence shows that one member of the STAT family, STAT3, has an additional property independent of its classical role in the nucleus. STAT3 modifed by serine phosphorylation augmented oxidative phosphorylation in mitochondria and supported cellular transformation by oncogenic Ras.
Joanna Wegrzyn, 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, and Andrew C. Larner (6 February 2009) Science323 (5915), 793.
[DOI: 10.1126/science.1164551] |Abstract »|Full Text »|PDF »|Supporting Online Material »
THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES:
Mouse hematopoietic cell-targeted STAT3 deletion: stem/progenitor cell defects, mitochondrial dysfunction, ROS overproduction, and a rapid aging-like phenotype.
C. Mantel, S. Messina-Graham, A. Moh, S. Cooper, G. Hangoc, X.-Y. Fu, and H. E. Broxmeyer (2012)
|Abstract »|Full Text »|PDF »
Targeting the Interleukin-6/Jak/Stat Pathway in Human Malignancies.