RT Journal Article
SR Electronic
T1 Identification of Ubiquitin Ligases Required for Skeletal Muscle Atrophy
JF Science
JO Science
FD American Association for the Advancement of Science
SP 1704
OP 1708
DO 10.1126/science.1065874
VO 294
IS 5547
A1 Bodine, Sue C.
A1 Latres, Esther
A1 Baumhueter, Susanne
A1 Lai, Venus K.-M.
A1 Nunez, Lorna
A1 Clarke, Brian A.
A1 Poueymirou, William T.
A1 Panaro, Frank J.
A1 Na, Erqian
A1 Dharmarajan, Kumar
A1 Pan, Zhen-Qiang
A1 Valenzuela, David M.
A1 DeChiara, Thomas M.
A1 Stitt, Trevor N.
A1 Yancopoulos, George D.
A1 Glass, David J.
YR 2001
UL http://science.sciencemag.org/content/294/5547/1704.abstract
AB Skeletal muscle adapts to decreases in activity and load by undergoing atrophy. To identify candidate molecular mediators of muscle atrophy, we performed transcript profiling. Although many genes were up-regulated in a single rat model of atrophy, only a small subset was universal in 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. Overexpression of MAFbx in myotubes produced atrophy, whereas mice deficient in either MAFbx orMuRF1 were found to be resistant to atrophy. These proteins are potential drug targets for the treatment of muscle atrophy.