In the labShowed that mTORC1 drives pyrimidine synthesis through S6K1 phosphorylation of CAD, and purine synthesis through ATF4-MTHFD2.
Own labBen-Sahra Lab, Northwestern University Feinberg School of Medicine (Chicago, Illinois, USA). He studies how growth signals tell cells to make more DNA and RNA building blocks, and how tumours exploit this. Signalling control of nucleotide and one-carbon/SAM metabolism by mTORC1 and MAPK/ERK in cancer.
Metabolism
Trained 1 person in this family ↓
Sources: 2013 (in the Atlas) · hsph.harvard.edu · doi.org
In the labFound nucleotide-synthesis dependencies of TSC-deficient, mTORC1-driven tumour cells that can be targeted.
Own labValvezan Lab, Rutgers CABM (Piscataway, New Jersey, USA). He looks for metabolic weak spots in tumours where mTOR is stuck 'on', so drugs can hit cancer cells and spare normal ones. How oncogenic signalling coordinates metabolic networks for growth, and how to exploit mTORC1-driven tumour dependencies such as purine synthesis.
Metabolism
Also trained with Peter S. Klein (PhD)
Sources: 2014 (in the Atlas) · PubMed 29183982 (2017) · cabm.rutgers.edu · hsph.harvard.edu
In the labFound links between PI3K-Akt-mTORC1 signalling and nucleotide and NADP/redox metabolism.
Own labChildren's Medical Center Research Institute (CRI), UT Southwestern Medical Center (Dallas, Texas, USA). She studies how growth signals manage the cell's 'charged batteries' (NAD and NADPH) that power building and defence. Signalling control of NAD(P) and redox metabolism in cancer and physiology.
Metabolism
Sources: 2014 (in the Atlas) · 2019 (in the Atlas) · cri.utsw.edu · hsph.harvard.edu
In the labIdentified TBC1D7 as the third core subunit of the TSC complex and studied mTORC2 regulation.
Own labDibble Lab, BIDMC & Harvard (Boston, Massachusetts, USA). He studies how growth signals control the cell's supply of coenzyme A, a molecule almost every metabolic reaction needs. PI3K signalling control of metabolism, especially a regulatory link between PI3K and coenzyme A synthesis.
Metabolism
Sources: 2012 (in the Atlas) · 2014 (in the Atlas) · hsph.harvard.edu · bbsphd.hms.harvard.edu
In the labThesis on liver mTORC1: showed that dietary protein, not insulin, is the main driver of liver mTORC1 after a meal.
Own labManning lab, Harvard T.H. Chan School of Public Health (Boston, Massachusetts, USA). She tested in mice what actually switches on mTOR in the liver after eating, and found that protein in the meal matters most. Physiological hierarchy of insulin, dietary protein and glucagon in liver and muscle mTORC1 regulation.
Metabolism
Sources: PubMed 41256362 (2025) · hsph.harvard.edu · cellbio.hms.harvard.edu
In the labShowed that insulin, through Akt phosphorylation of TSC2, makes the TSC complex leave the lysosome so Rheb can switch on mTORC1 (Cell 2014).
Own labProfile, Manning Lab (Harvard Chan) (Boston, Massachusetts, USA). She showed that insulin works partly by moving the mTOR 'brake' (TSC) away from where mTOR sits. Spatial control of the TSC complex and mTORC1 at the lysosome; later drug-discovery biology.
mTORC1 nutrient sensing
Sources: 2014 (in the Atlas) · 2012 (in the Atlas) · hsph.harvard.edu · doi.org
