MG53-induced IRS-1 ubiquitination negatively regulates skeletal myogenesis and insulin signalling
Published 2013 View Full Article
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Title
MG53-induced IRS-1 ubiquitination negatively regulates skeletal myogenesis and insulin signalling
Authors
Keywords
-
Journal
Nature Communications
Volume 4, Issue 1, Pages -
Publisher
Springer Nature
Online
2013-08-22
DOI
10.1038/ncomms3354
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- (2013) Ruisheng Song et al. NATURE
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- (2011) Carey N. Lumeng et al. JOURNAL OF CLINICAL INVESTIGATION
- Transcriptional mechanisms regulating skeletal muscle differentiation, growth and homeostasis
- (2011) Thomas Braun et al. NATURE REVIEWS MOLECULAR CELL BIOLOGY
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- (2010) C. Chambon et al. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
- Ginsenoside Rh2 induces ligand-independent Fas activation via lipid raft disruption
- (2009) Jae-Sung Yi et al. BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
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- Leptin Administration Favors Muscle Mass Accretion by Decreasing FoxO3a and Increasing PGC-1α in ob/ob Mice
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- MG53 nucleates assembly of cell membrane repair machinery
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- (2008) Marco Sandri PHYSIOLOGY
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