The IGF-1/PI3K/Akt pathway prevents expression of muscle atrophy-induced ubiquitin ligases by inhibiting FOXO transcription factors.

By T. Stitt, D. Drujan, B. A. Clarke, Frank J. Panaro, Yekatarina Timofeyva, W. O. Kline, Michael Gonzalez, G. Yancopoulos, D. Glass. Molecules and Cells, 2004

1,965 citations recorded by the source corpus.

Subfields: Geriatrics and Gerontology, Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/1fde9dcce0505fa32a0d75942885bd7c76d859db

How researchers see this paper

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

In Geriatrics and Gerontology

1. M. Sandri
2. E. L. Greer
3. D. Accili
4. A. Brunet
5. R. DePinho
6. S. Manolagas
7. Hilmar Bading
8. G. Hardingham

In Molecular Biology

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

In Physiology

1. M. Sandri
2. S. Schiaffino
3. P. Bonaldo
4. D. Glass
5. D. Clegg
6. M. Birnbaum
7. Rute Martins
8. A. V. D. Heuvel

Citations in the corpus

• FoxOs at the crossroads of cellular metabolism, differentiation, and transformation. (2004, positive): “These observation prevents their induction, opening a new front in thetions dovetail with the antidifferentiative effects FoxO3a struggle to treat muscular atrophy (Sandri et al., 2004;in the female gonad, as described above (Castrillon et Stitt et al., 2004).”
• The role of FoxO in the regulation of metabolism (2008, background): “The increased expression of atrogin-1 and MuRF-1, as well as the subsequent atrophy that ensues, is antagonized by IGF-1 or overexpression of active PI3K or Akt (Sandri et al., 2004; Stitt et al., 2004).”
• FOXO transcription factors at the interface between longevity and tumor suppression (2005, background): “Atrophy In fully differentiated skeletal and cardiac muscle cells, expression of a constitutively active form of FOXO3 causes atrophy (Sandri et al., 2004; Stitt et al., 2004; Skurk et al., 2005).”
• The E3 Ligase MuRF1 degrades myosin heavy chain protein in dexamethasone-treated skeletal muscle. (2007, methodology): “…a previously described cell culture model of muscle atrophy was employed, in which C2C12 myotubes are treated with the synthetic glucocorticoid dexamethasone (DEX), resulting in phenotypic atrophy as determined by measuring myotube diameter and the loss of insoluble protein (Stitt et al., 2004).”
• FoxO1 protects against pancreatic beta cell failure through NeuroD and MafA induction. (2005, neutral): “, 1999) or cellular atrophy (Sandri et al., 2004; Stitt et al., 2004).”
• Transcriptional mechanisms regulating skeletal muscle differentiation, growth and homeostasis (2011, background): “Recently, the expression of catabolic genes was found to be regulated by the transcription factor forkhead box O1 (FOXO1) and FOXO3”
• Mitochondrial fission and remodelling contributes to muscle atrophy (2010, background): “Expression of the fission machinery is per se sufficient to cause muscle wasting in adult animals, by triggering organelle dysfunction and AMPK activation.”
• Pharmacologic disruption of Polycomb-repressive complex 2-mediated gene repression selectively induces apoptosis in cancer cells. (2007, background): “The role of FBXO32 in negatively regulating cell survival has been implicated in a previous finding showing that its expression could be inhibited by the prosurvival PI3K/Akt pathway (Stitt et al. 2004).”
• Regulation of autophagy and the ubiquitin–proteasome system by the FoxO transcriptional network during muscle atrophy (2015, positive): “We have recently established that these atrophy-related ubiquitin ligases, as well as protein breakdown in general, are blocked by the growth-promoting IGF1/AKT pathway 8,9 .”