Alexander J. Valvezan
Showed as a Manning-lab postdoc that mTORC1 matches nucleotide production to demand, creating a weak point that can be targeted in tumours with TSC loss. His Rutgers lab found that mTORC1 activity rises and falls through the cell cycle and helps drive entry into mitosis
Assistant Professor of Pharmacology, Rutgers Robert Wood Johnson Medical School · postdoc, Harvard T.H. Chan School of Public Health (Brendan Manning lab) · PhD, University of Pennsylvania
Valvezan Lab, Rutgers CABM (Piscataway, New Jersey, USA) ↗ Lab lineagetrained under Brendan D. Manning → Bluesky@alexandervalvezan.bsky.social ↗ ORCID0000-0002-4369-6074 ↗
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
A selection, not a full bibliography: only papers that meet the Atlas inclusion criteria.
| Year | Evidence | Study |
|---|---|---|
| 2014 | M | Spatial control of the TSC complex integrates insulin and nutrient regulation of mTORC1 at the lysosome MEN2014 Spatial control of the TSC complex integrates insulin and nutrient inputs at the lysosome. |
| 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. |
Co-authors in the Atlas 10
People with a profile here who share at least one study with Alexander J. Valvezan.
ShowHide
- Brendan D. Manning 3 shared studies Was among the groups that in 2002 identified TSC2 as a direct target of Akt (MAN2002), linking insulin and PI3K signalling to mTORC1, and later found TBC1D7 as the third subunit of the TSC complex. His lab has shown how mTORC1 turns growth signals into the synthesis of lipids and nucleotides
- David J. Kwiatkowski Geneticist and physician who studies tuberous sclerosis complex (TSC) and the TSC1/TSC2 genes that restrain mTORC1.
- George Talbott Research assistant in Brendan Manning's mTOR lab at Harvard in 2013 and 2014, who contributed to studies on where the TSC complex sits in the cell and how metformin reaches mTORC1
- Gerta Hoxhaj Studies how growth signalling through PI3K, AKT and mTOR rewires cell metabolism; as a Manning-lab postdoc she co-authored work on how metformin inhibits mTORC1 in the liver
- Christian C. Dibble Identified TBC1D7 as the third subunit of the TSC complex that controls mTORC1, as a Manning-lab graduate student. His lab at Beth Israel Deaconess studies how PI3K signalling and nutrient supply are integrated to control mTORC1 and cell metabolism
- Jay N. Joshi Showed mTORC1 activity itself rises and falls across the cell cycle, not just in response to nutrients
- John M. Asara Mass-spectrometry specialist whose core facility supplied metabolomics and proteomics for several mTOR studies, including measurements of purine, pyrimidine and SAM metabolism downstream of mTORC1.
- Lewis C. Cantley Co-discovered PI3K, the pathway that feeds into mTOR from growth factors
- Marc Turner Research assistant and lab manager in Brendan Manning's mTOR lab at Harvard from 2014 to 2016, who contributed to studies on nucleotide synthesis in tumour cells and on metformin's route to mTORC1
- Sue Menon Showed insulin controls mTORC1 by moving the TSC complex on and off the lysosome
Every researcher with a profile →
Thank you. That helps us know which pages have been read by someone who knows the work.
Thank you. We will check it and correct the page.
Thank you. Your answer was counted anonymously.