Foxo transcription factors induce the atrophy-related ubiquitin ligase atrogin-1 and cause skeletal muscle atrophy.

By M. Sandri, C. Sandri, A. Gilbert, Carsten Skurk, E. Calabria, Anne Picard, K. Walsh, S. Schiaffino, S. Lecker, A. Goldberg. Cell, 2004

2,963 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/1d11dfe843198a0a31560f90c5b783d2b85f5cb6

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Citations in the corpus

Reversal of cancer cachexia and muscle wasting by ActRIIB antagonism leads to prolonged survival. (2010, background): “While activation of the AKT pathway is associated with muscle growth, in atrophying muscles there is an activation of FOXO as well as NF-kB and possibly also Smad transcription factors, which promote protein degradation (Glass, 2005; Sandri et al., 2004).”
FOXO/4E-BP Signaling in Drosophila Muscles Regulates Organism-wide Proteostasis During Aging (2010, result): “There is an apparent contradiction between our findings and the data describing the FOXO-dependent induction of muscle atrophy inmice (Bodine et al., 2001; Sandri et al., 2004), a serious form of muscle degeneration that results in decreased muscle strength (Augustin and Partridge, 2009).”
Mitochondrial fission and remodelling contributes to muscle atrophy (2010, methodology): “These promoters have been already shown to contain the major regulatory elements for the correct upregulation of these ubiquitin ligases in atrophying muscles (Sandri et al, 2004; Mammucari et al, 2007; Sandri, 2008; Sartori et al, 2009).”
Autophagy is required to maintain muscle mass. (2009, positive): “Expression of several atrophyrelated genes, including MuRF1, cathepsin L, and Bnip3l, were more upregulated in atrophying muscles of Atg7 / muscles, which suggest a more important activation of the atrophy program (Figures 3B and S16).”
Fiber types in mammalian skeletal muscles. (2011, background): “The FoxO transcription factors, in particular FoxO3, control muscle atrophy by activating the ubiquitin-proteasome (693) and the autophagy-lysosome pathways (518, 895).”
Cancer cachexia: mediators, signaling, and metabolic pathways. (2012, background): “PGC-1a is itself downregulated in muscles from tumor-bearing mice and other wasting conditions, and transgenic expression of PGC-1a rescues muscle loss in part by inhibiting Foxo3 and through the production of metabolic products.”
FoxO3 coordinately activates protein degradation by the autophagic/lysosomal and proteasomal pathways in atrophying muscle cells. (2007, background): “When expressed at a level similar to ca-FoxO3, wild-type FoxO3 (wt-FoxO3) increased the rate of proteolysis by only 15% (Figure 1B, p < 0.01), presumably because most of the wt-FoxO3 was phosphorylated by Akt and inactive (Brunet et al., 1999; Sandri et al., 2004).”
FoxO transcription factors in the maintenance of cellular homeostasis during aging. (2008, background): “ZNF216, a novel ubiquitin-binding protein containing a zinc-finger), resulting in skeletal muscle atrophy without apoptosis [66 ,67 ,68,69].”
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”
The SCF ubiquitin ligase: insights into a molecular machine (2004, background): “pl?Q969P5">Fbx32 (also known as Mafbx or Atrogin1) is the product of one of only two genes that are upregulated in a panel of rat models of muscle atroph”
The role of FoxO in the regulation of metabolism (2008, background): “Overexpression of FoxO3a also increases the activity of the atrogin-1 promoter both in vitro and in vivo, and transgenic overexpression of FoxO1 in skeletal muscle results in severe muscular atrophy (Kamei et al., 2004; Sandri et al., 2004; Southgate et al., 2007).”
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).”