mTORC1 Couples Nucleotide Synthesis to Nucleotide Demand Resulting in a Targetable Metabolic Vulnerability

The mechanistic target of rapamycin complex 1 (mTORC1) supports proliferation through parallel induction of key anabolic processes, including protein, lipid, and nucleotide synthesis. We hypothesized that these processes are coupled to maintain anabolic balance in cells with mTORC1 activation, a common event in human cancers. Loss of the tuberous sclerosis complex (TSC) tumor suppressors results in activation of mTORC1 and development of the tumor syndrome TSC.

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Valvezan, A. J., et al. (2017). mTORC1 Couples Nucleotide Synthesis to Nucleotide Demand Resulting in a Targetable Metabolic Vulnerability. Cancer cell. https://doi.org/10.1016/j.ccell.2017.09.013

@article{VAL2017,
  author       = {Valvezan, A. J. and Manning, B. D. and others},
  title        = {{mTORC1 Couples Nucleotide Synthesis to Nucleotide Demand Resulting in a Targetable Metabolic Vulnerability}},
  journal      = {Cancer cell},
  year         = {2017},
  doi          = {10.1016/j.ccell.2017.09.013},
  note         = {PMID: 29056426},
}

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 VAL2017) [Data set]. https://mtor-atlas.org/study/VAL2017/ · Dataset DOI 10.5281/zenodo.22059963

@misc{atlas_VAL2017,
  author       = {Barton, Oliver},
  title        = {{Oliver's mTOR Atlas}, record VAL2017},
  howpublished = {Data set},
  year         = {2026},
  url          = {https://mtor-atlas.org/study/VAL2017/},
  doi          = {10.5281/zenodo.22059963}
}