FoxO3 controls autophagy in skeletal muscle in vivo.

By C. Mammucari, G. Milan, V. Romanello, E. Masiero, Ruediger Rudolf, P. del Piccolo, S. Burden, R. Di Lisi, C. Sandri, Jinghui Zhao and 3 more. Cell Metabolism, 2007

1,961 citations recorded by the source corpus.

Subfields: Epidemiology, Geriatrics and Gerontology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/7252f79fac2c62efc57b5d6303b10107042afeed

How researchers see this paper

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

In Epidemiology

1. Beth Levine
2. I. Slaninová
3. Guido Kroemer
4. D. Klionsky
5. N. Mizushima
6. V. Deretic
7. Douglas R. Green
8. Alec C. Kimmelman

In Geriatrics and Gerontology

1. R. Shaw
2. Derek P. Narendra
3. M. Sandri
4. D. Klionsky
5. V. Deretic
6. Guido Kroemer
7. S. Minucci
8. A. Brunet

In Molecular Biology

1. Beth Levine
2. I. Slaninová
3. Guido Kroemer
4. M. Sandri
5. D. Klionsky
6. Douglas R. Green
7. Alec C. Kimmelman
8. S. Schiaffino

Citations in the corpus

• Cancer cachexia: mediators, signaling, and metabolic pathways. (2012, background): “TORC2 signaling controls autophagy, which also plays a role in muscle maintenance (Mammucari et al., 2007; Mieulet et al., 2007; Zhao et al., 2007).”
• During muscle atrophy, thick, but not thin, filament components are degraded by MuRF1-dependent ubiquitylation (2009, background): “Recent findings indicate that these different types of atrophy activate a common series of biochemical and transcriptional adaptations (Sacheck et al., 2007) leading to enhanced protein degradation by both proteasomal and lysosomal systems (Mammucari et al., 2007; Zhao et al., 2007).”
• Autophagy is required to maintain muscle mass. (2009, positive): “Excessive activation of autophagy aggravates muscle wasting (Dobrowolny et al., 2008; Mammucari et al., 2007; Wang et al., 2005; Zhao et al., 2007) by removing portion of cytoplasm, proteins, and organelles.”
• Reversal of cancer cachexia and muscle wasting by ActRIIB antagonism leads to prolonged survival. (2010, background): “FOXO3 activation has been shown to induce Atrogin-1 and MuRF1 transcription, stimulate proteolysis and cause atrophy (Mammucari et al., 2007; Sandri et al., 2004; Zhao et al., 2007).”
• FoxO3 coordinately activates protein degradation by the autophagic/lysosomal and proteasomal pathways in atrophying muscle cells. (2007, background): “Also,increased formation of autophagosomes labeled by GFP-LC3 has recently been demonstrated in mouse muscles upon fasting (Mizushima et al., 2004) and denervation (Mammucari et al., 2007 [this issue of Cell Metabolism ]).”
• Mechanisms of IGF-1-Mediated Regulation of Skeletal Muscle Hypertrophy and Atrophy (2020, background): “Autophagy is regulated by two main pathways that overlap with IGF-1 signaling pathways: mTOR-mediated inhibitory phosphorylation of unc51-like kinase-1 (ULK1) and FoxO3-mediated induction of autophagy-related genes.”
• Defective Hepatic Autophagy in Obesity Promotes ER Stress and Causes Insulin Resistance (2010, background): “Finally, autophagy is regulated by the integrated actions of insulin and mTOR (Ellington et al., 2006; Mammucari et al., 2007; Xie and Klionsky, 2007), both of which are altered in obesity.”
• Autophagy and the integrated stress response (2010, positive): “Following its dephosphorylation, FOXO3 translocates into the nucleus (Figure 3A) and upregulates multiple autophagy-related genes such as ULK2, Beclin 1, VPS34, BNIP3 and BNIP3L, ATG12, ATG4B, LC3, and GABARAPL1 (Mammucari et al., 2007).”