Alexander J. Valvezan
Mapped how mTORC1 couples nucleotide synthesis to a cell's building needs
PhD, University of Pennsylvania · postdoc, Harvard T.H. Chan School of Public Health (Brendan Manning lab) · Assistant Professor of Pharmacology, Rutgers Robert Wood Johnson Medical School
Valvezan Lab, Rutgers CABM ↗ Bluesky@alexandervalvezan.bsky.social ↗
Portrait: Center for Advanced Biotechnology and Medicine, Rutgers
Alexander Valvezan trained as a postdoc in Brendan Manning's lab at Harvard, where he worked out how mTORC1 links cell-growth signals to the metabolic pathways that build the nucleotides a growing or dividing cell needs.
His 2017 Cancer Cell paper showed that mTORC1 couples nucleotide synthesis to nucleotide demand, and that disrupting this coupling creates a targetable metabolic vulnerability in tumours with hyperactive mTORC1 signalling, such as those driven by loss of the TSC1/TSC2 tumour suppressors. He now runs his own lab at Rutgers, studying how mTORC1 coordinates metabolic networks and how oncogenic mutations can be exploited therapeutically.
The timeline below follows Valvezan's contributions gathered in this Atlas.
Milestones in the Atlas
| Year | Evidence | Study |
|---|---|---|
| 2017 | M | mTORC1 Couples Nucleotide Synthesis to Nucleotide Demand Resulting in a Targetable Metabolic Vulnerability VAL2017 Shows mTORC1 couples nucleotide synthesis to nucleotide demand, revealing a targetable metabolic vulnerability in tumours with hyperactive mTORC1. |
| 2019 | R | Molecular logic of mTORC1 signalling as a metabolic rheostat VAL2019 Reviews the molecular logic of mTORC1 signalling as a metabolic rheostat. |
| 2024 | M | mTORC1 activity oscillates throughout the cell cycle, promoting mitotic entry and differentially influencing autophagy induction JOS2024 Shows mTORC1 activity oscillates through the cell cycle, promoting mitotic entry and differentially influencing autophagy induction. |