AMP-activated protein kinase induces a p53-dependent metabolic checkpoint.

By Russell G. Jones, D. Plas, Sara P. Kubek, M. Buzzai, J. Mu, Yang Xu, M. Birnbaum, Craig B. Thompson. Molecules and Cells, 2005

1,645 citations recorded by the source corpus.

Subfields: Epidemiology, Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/d7ac7ad912e5dbe5c8bda9bd18e1710f6af66108

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Citations in the corpus

Metabolic Reprogramming: A Cancer Hallmark Even Warburg Did Not Anticipate (2012, background): “Consistent with this hypothesis, activation of the tumor suppressor p53 has been shown to be critical for cell survival following glucose depletion (Jones et al., 2005).”
p53 in health and disease (2007, background): “Metabolic stress that results in low glucose levels has been shown to activate p53 through a pathway that involves AMP kinase (AMPK), and has been proposed to contribute to the short-term survival of cells suffering, hopefully temporary, starvatio”
The energy sensing LKB1–AMPK pathway regulates p27kip1 phosphorylation mediating the decision to enter autophagy or apoptosis (2007, background): “AMPK, which is activated by AMP and the Peutz-Jeghers syndrome gene product LKB1, functions as an intracellular energy sensor regulating metabolism and cell proliferation through phosphorylation of acetyl CoA carboxylase (ACC) and tumour suppressors, including tuberin (TSC2) and p53 (ref”
AMPK is a negative regulator of the Warburg Effect and suppresses tumor growth in vivo (2012, methodology): “We and others have established that AMPK is the central mediator of a metabolic cell-cycle checkpoint activated in response to nutrient limitation in mammalian cells (Gwinn et al., 2008; Inoki et al., 2003; Jones et al., 2005).”
Cancer Cell Metabolism: One Hallmark, Many Faces (2012, background): “Finally, it is worth noting that p53 also functions in a positive feedback loop with AMPK, whereby p53 can transcriptionally enhance the AMPK-dependent cellular stress response, while AMPK can catalyze the activation-initiating phosphorylation of p53 (69, 70).”
LKB1 and AMPK control of mTOR signalling and growth (2009, background): “The tumour suppressor p53 (Jones et al. 2005) and the CDK inhibitor protein p27 (Liang et al. 2007) have been reported to be direct substrates of AMPK, though neither of the reported AMPK phosphorylation sites in these proteins exactly conform to the established optimal substrate motif for AMPK,…”
Systemic treatment with the antidiabetic drug metformin selectively impairs p53-deficient tumor cell growth. (2007, background): “However, a recent study revealed a prosurvival role for p53 in cells metabolically impaired by glucose limitation (12).”
The energy sensor AMPK regulates T cell metabolic adaptation and effector responses in vivo. (2015, background): “The reversible metabolic checkpoint induced in lymphocytes is reminiscent of AMPK function in tumor cells, where AMPK triggers a cell cycle checkpoint to maintain cell viability under poor nutrient conditions (Jones et al., 2005).”
Doxorubicin: an update on anticancer molecular action, toxicity and novel drug delivery systems (2013, background): “A recent study highlighted AMPK as being the most important upstream signal for the phosphorylation of p53 at serine 15, as well as its activation in the presence of doxorubicin, ultimately causing programmed cell death and arresting the cell cycle.([25,26,39])”
The regulation of AMPK beta1, TSC2, and PTEN expression by p53: stress, cell and tissue specificity, and the role of these gene products in modulating the IGF-1-AKT-mTOR pathways. (2007, methodology): “In the presence of such stress signals, the p53 pathway shuts down both the IGF-1-AKT pathway and mTOR pathway (2, 22, 23).”