Rapid disuse and denervation atrophy involve transcriptional changes similar to those of muscle wasting during systemic diseases

By J. Sacheck, J. Hyatt, A. Raffaello, R. Thomas Jagoe, Roland R. Roy, V. Reggie Edgerton, S. Lecker, A. Goldberg. The FASEB Journal, 2007

599 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/bec4b6995d308fb001100ce3b411dcce674ee4ad

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cellular and Molecular Neuroscience

1. M. Sandri
2. S. Schiaffino
3. A. Goldberg
4. S. Lecker
5. C. Mammucari
6. L. Scorrano
7. D. Glass

In Molecular Biology

1. M. Sandri
2. S. Schiaffino
3. P. Bonaldo
4. C. Mammucari
5. A. Goldberg
6. E. Masiero
7. S. Lecker
8. V. Romanello

In Physiology

1. M. Sandri
2. S. Schiaffino
3. P. Bonaldo
4. M. Birnbaum
5. A. V. D. Heuvel
6. David H. Gross

Citations in the corpus

• The role of FoxO in the regulation of metabolism (2008, background): “It remained elevated and is presumed to play a role not only in inducing the atrophy state but also in maintaining it (Sacheck et al., 2007).”
• Mitochondrial fission and remodelling contributes to muscle atrophy (2010, background): “…days 21 days &2010 European Molecular Biology Organization The EMBO Journal VOL 29 | NO 10 | 2010 1781 many forms of muscle wasting expression of a variety of genes for enzymes important in glycolysis and oxidative phosphorylation are also suppressed co-ordinately (Sacheck et al, 2007).”
• FoxO3 coordinately activates protein degradation by the autophagic/lysosomal and proteasomal pathways in atrophying muscle cells. (2007, background): “We have previously identified a set of atrophy-specific genes or ‘‘atrogenes’’ that are up-or downregulated similarly in muscles in these diverse types of atrophy (Lecker et al., 2004; Sacheck et al., 2007).”
• FoxO3 controls autophagy in skeletal muscle in vivo. (2007, methodology): “…of the ubiquitin-proteasome system and found that the two protein degradation pathways are The key ubiquitin ligases atrogin-1 and MuRF1 and several other genes of the ubiquitin-proteasome system are upregulated in different models of muscle wasting (Bodine et al., 2001a; Sacheck et al., 2007).”
• Cellular and molecular mechanisms of muscle atrophy (2013, background): “Because the diverse disease models used for these microarray experiments (including diabetes, cancer cachexia, chronic renal failure, fasting and denervation) have muscle atrophy in common, the commonly up- or downregulated genes are believed to regulate the loss of muscle components and are called ”