The TWEAK–Fn14 system is a critical regulator of denervation-induced skeletal muscle atrophy in mice
Open Access
- 22 March 2010
- journal article
- Published by Rockefeller University Press in The Journal of cell biology
- Vol. 188 (6), 833-849
- https://doi.org/10.1083/jcb.200909117
Abstract
The TNF-related cytokine TWEAK promotes skeletal muscle atrophy that is associated with classical disuse syndromes.Keywords
This publication has 54 references indexed in Scilit:
- During muscle atrophy, thick, but not thin, filament components are degraded by MuRF1-dependent ubiquitylationThe Journal of cell biology, 2009
- Matrix metalloproteinase-9 inhibition ameliorates pathogenesis and improves skeletal muscle regeneration in muscular dystrophyHuman Molecular Genetics, 2009
- A Novel Role for Tumor Necrosis Factor–Like Weak Inducer of Apoptosis (TWEAK) in the Development of Cardiac Dysfunction and FailureCirculation, 2009
- Tumor Necrosis Factor-related Weak Inducer of Apoptosis Augments Matrix Metalloproteinase 9 (MMP-9) Production in Skeletal Muscle through the Activation of Nuclear Factor-κB-inducing Kinase and p38 Mitogen-activated Protein KinaseOnline Journal of Public Health Informatics, 2009
- Sarcolemma-localized nNOS is required to maintain activity after mild exerciseNature, 2008
- Nuclear factor-kappa B signaling in skeletal muscle atrophyJournal of Molecular Medicine, 2008
- The TWEAK–Fn14 cytokine–receptor axis: discovery, biology and therapeutic targetingNature Reviews Drug Discovery, 2008
- Myosin accumulation and striated muscle myopathy result from the loss of muscle RING finger 1 and 3JCI Insight, 2007
- TWEAK, via its receptor Fn14, is a novel regulator of mesenchymal progenitor cells and skeletal muscle regenerationThe EMBO Journal, 2006
- Targeted ablation of IKK2 improves skeletal muscle strength, maintains mass, and promotes regenerationJCI Insight, 2006