The coordinate regulation of the p53 and mTOR pathways in cells.

By Zhaohui Feng, Haiyan Zhang, Arnold J. Levine, Shengkan Jin. Proceedings of the National Academy of Sciences of the United States of America, 2005

1,244 citations recorded by the source corpus.

Subfields: Epidemiology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/981af41c1d729ae75fc11106b583b6d143896133

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Citations in the corpus

Mitochondria in cancer cells: what is so special about them? (2008, positive): “Indeed, an interesting relationship betweenp53 and glucose metabolism has recently been established [28, 29 ].”
Genomic instability — an evolving hallmark of cancer (2010, background): “, this hallmark could be expanded to include senescence, and possibly even other forms of p53-mediated cell death, such as autophag”
ATM signals to TSC2 in the cytoplasm to regulate mTORC1 in response to ROS (2010, background): “Although mTORC1 repression in response to DNA damage has been observed previously (18, 19), and has recently been linked to activation of p53 (20, 21), a mechanism for repression of mTORC1 in response to oxidative damage had not previously been elucidated.”
Bif-1 interacts with Beclin 1 through UVRAG and regulates autophagy and tumorigenesis (2007, background): “In addition, oncogenes (such as Akt and Bcl-2) suppress autophagy, whereas tumour suppressors (such as DAPK, p53 and PTEN) stimulate autophag”
Tumor suppressors and cell metabolism: a recipe for cancer growth. (2009, background): “Moreover, p53 activation can reinforce AMPK-dependent responses through a series of p53-dependent feedback loops that in turn activate AMPK (Feng et al. 2005; Budanov and Karin 2008).”
Role of autophagy in cancer (2007, background): “These responses might vary with cell type and type of stress, and will undoubtedly reflect the nature of the mutational events that have occurred in the tumour cells, not only that of BECN1 and the PI3K pathway as described above, but also p53 statu”
MicroRNA-34b and MicroRNA-34c are targets of p53 and cooperate in control of cell proliferation and adhesion-independent growth. (2007, methodology): “Towards this aim, we took advantage of the p53MH algorithm (17), which has previously identified novel p53responsive genes (22), to search 5 kb upstream and downstream of each down-regulated miRNA.”
Autophagy in the pathogenesis of disease. (2008, positive): “P53, the most commonly mutated tumor suppressor gene in human cancers, positively regulates autophagy in DNA-damaged cells, perhaps through AMPK activation of the TSC1/TSC2 complex and subsequent TOR inhibition or perhaps via upregulation of DRAM (damageregulated autophagy modulator), a lysosomal pr”
mTOR signaling in growth control and disease (2012, positive): “DNA damage induces the expression of Tsc2 and phosphatase and tensin homolog deleted on chromosome 10 (Pten), causing downregulation of the entire PI3K-mTORC1 axis (Feng et al., 2005; Stambolic et al., 2001), and activates AMPK through a mechanism that depends on the induction of Sestrin1/2 (Budanov”
The dynamic nature of autophagy in cancer. (2011, background): “This can be through inhibition of mTOR (Feng et al. 2005) or by activation of DRAM (damage-regulated autophagy modulator) (Crighton et al. 2006).”
Self-eating and self-killing: crosstalk between autophagy and apoptosis (2007, background): “In one study, p53 was linked to autophagy through mTOR inhibition via AMPK and the tumour suppressors tuberous sclerosis-1 (TSC1) and TSC2 (Ref”
p53 target genes sestrin1 and sestrin2 connect genotoxic stress and mTOR signaling. (2008, positive): “p53 also increases the phosphorylation of the AMPKa subunit, leading to AMPK activation (Feng et al., 2005).”