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Biotech / Medical : Regeneron Pharmaceuticals -- Ignore unavailable to you. Want to Upgrade?

To: Miljenko Zuanic who wrote (584)	10/27/2001 3:11:36 PM
From: Miljenko Zuanic	Read Replies (1) \| Respond to of 3559

Science 2001 Oct 25 Published online October 25, 2001 Submitted on August 30, 2001 Accepted on October 17, 2001 Identification of Ubiquitin Ligases Required for Skeletal Muscle Atrophy Sue C. Bodine 1, Esther Latres 1, Susanne Baumhueter 2, Venus K.-M. Lai 1, Lorna Nunez 1, Brian A. Clarke 1, William T. Poueymirou 1, Frank J. Panaro 1, Erqian Na 1, Kumar Dharmarajan 1, Zhen-Qiang Pan 3, David M. Valenzuela 1, Thomas M. DeChiara 1, Trevor N. Stitt 1, George D. Yancopoulos 1, David J. Glass 1* 1 Regeneron Pharmaceuticals, 777 Old Saw Mill River Road, Tarrytown, NY, 10591-6707, USA. 2 Applied Biosystems, 850 Lincoln Center Drive, Foster City, CA 94404, USA. 3 Derald H. Ruttenberg Cancer Center, Mount Sinai School of Medicine, New York, NY, 10029-6574, USA. * To whom correspondence should be addressed. E-mail: david.glass@regeneron.com. Skeletal muscle adapts to decreases in activity and load by undergoing atrophy. To define candidate molecular mediators of muscle atrophy, we performed transcript profiling. Although many genes were upregulated in a single rat model of atrophy, only a small subset was universal to all atrophy models. Two of these genes encode ubiquitin ligases: Muscle RING Finger 1 (MuRF1), and a gene we designate Muscle Atrophy F-box (MAFbx), the latter being a member of the "SCF" family of E3 ubiquitin ligases. Over-expression of MAFbx in myotubes produced atrophy, while mice deficient in either MAFbx or MuRF1 were found to be resistant to atrophy. These proteins represent potential novel drug targets for the treatment of muscle atrophy.