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

Jones RG, Plas DR, Kubek S, Buzzai M, Mu J, Xu Y, Birnbaum MJ, Thompson CB · 2005 · Molecular Cell · Atlas ID JON2005

What this study shows

Described a glucose checkpoint at the G1/S boundary run by AMPK. Cells arrested when glucose ran short even though amino acids were present and mTOR stayed active, so this arrest works in parallel to mTOR rather than through it. AMPK phosphorylated p53 on serine 15, which was needed for the arrest; arrested cells re-entered the cycle when glucose returned, while persistent AMPK activation pushed them into p53-dependent senescence. Boundary: worked from the abstract only (no PMC full text); cultured cells.

Abstract

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Replicative cell division is an energetically demanding process that can be executed only if cells have sufficient metabolic resources to support a doubling of cell mass. Here we show that proliferating mammalian cells have a cell-cycle checkpoint that responds to glucose availability. The glucose-dependent checkpoint occurs at the G(1)/S boundary and is regulated by AMP-activated protein kinase (AMPK). This cell-cycle arrest occurs despite continued amino acid availability and active mTOR.

Read the full abstract on PubMed →

At a glance

Evidence type	M Molecular — cells, biochemistry, structure Marked M because it is molecular or in-vitro work (model: Proliferating mammalian cells under glucose deprivation; p53 serine-15 mutant cells) rather than a whole-organism health-outcome study. That is often exactly where causal biology gets established -- the code says which system the finding was shown in, and nothing about how good the work is.
Study type	5 - Mechanistic / In Vitro
Model system	Proliferating mammalian cells under glucose deprivation; p53 serine-15 mutant cells
Journal	Molecular Cell
Year	2005
Peer reviewed	Yes
Record last updated	2026-10-01
Source	DOI 10.1016/j.molcel.2005.03.027 · PMID 15866171

Extracted findings

These fields were extracted from the paper with AI assistance and have not been checked against the source. Read them as a pointer into the paper, not as curated claims; where they disagree with the curated summary above, the curated summary stands.

Intervention	Glucose deprivation; AMPK activation
Target	AMPK -> p53 (Ser15)
Model	Mammalian cell lines
Effect	AMPK imposes a reversible p53-dependent G1/S arrest; sustained activation leads to senescence

In the Atlas

Cite this paper

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Jones, R. G., Plas, D. R., Kubek, S., Buzzai, M., Mu, J., Xu, Y., Birnbaum, M. J., & Thompson, C. B. (2005). AMP-activated protein kinase induces a p53-dependent metabolic checkpoint. Molecular Cell. https://doi.org/10.1016/j.molcel.2005.03.027

@article{JON2005,
  author       = {Jones, R. G. and Plas, D. R. and Kubek, S. and Buzzai, M. and Mu, J. and Xu, Y. and Birnbaum, M. J. and Thompson, C. B.},
  title        = {{AMP-activated protein kinase induces a p53-dependent metabolic checkpoint}},
  journal      = {Molecular Cell},
  year         = {2005},
  doi          = {10.1016/j.molcel.2005.03.027},
  note         = {PMID: 15866171},
}

Cite this Atlas record

The record is the Atlas's own work — the evidence label, the extracted findings and the links. It is cited as part of the dataset, not as the paper.

Barton, O. (2026). Oliver's mTOR Atlas (record JON2005) [Data set]. https://mtor-atlas.org/study/JON2005/ · Dataset DOI 10.5281/zenodo.22059963

@misc{atlas_JON2005,
  author       = {Barton, Oliver},
  title        = {{Oliver's mTOR Atlas}, record JON2005},
  howpublished = {Data set},
  year         = {2026},
  url          = {https://mtor-atlas.org/study/JON2005/},
  doi          = {10.5281/zenodo.22059963}
}

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