Diane C. Fingar
Studies how mTORC1 and mTORC2 are regulated, especially through site-specific phosphorylation
Professor of Cell and Developmental Biology · Associate Chair · University of Michigan Medical School
Portrait: University of Michigan Medical School
Diane Fingar is Professor of Cell and Developmental Biology at the University of Michigan Medical School, where she is also Associate Chair of the department. Her lab studies how the two mTOR complexes, mTORC1 and mTORC2, are switched on and off, especially through phosphorylation at specific sites, and how they talk to other signalling systems.
She earned her PhD at Harvard Medical School (1995), did postdoctoral work at Massachusetts General Hospital and Harvard Medical School, and was an Instructor in Cell Biology at Harvard before moving to Michigan.
In the Atlas she is first author of FIN2002 from John Blenis's lab. It showed that mammalian cell size depends on mTOR, separately from cell division, and that mTOR controls size through two downstream targets, S6K1 and the 4E-BP1/eIF4E pair.
Milestones in the Atlas
A selection, not a full bibliography: only papers that meet the Atlas inclusion criteria.
| Year | Evidence | Study |
|---|---|---|
| 2002 | M | Mammalian cell size is controlled by mTOR and its downstream targets S6K1 and 4EBP1/eIF4E FIN2002 First author: mTOR sets mammalian cell size through S6K1 and 4E-BP1/eIF4E, separately from cell-cycle progression (cells). |
| 2002 | M | Tuberous sclerosis complex-1 and -2 gene products function together to inhibit mammalian target of rapamycin (mTOR)-mediated downstream signaling TEE2002 Co-author: the TSC1–TSC2 complex inhibits mTOR signalling to S6K1 and 4E-BP1 (cells). |
| 2003 | M | TOS motif-mediated raptor binding regulates 4E-BP1 multisite phosphorylation and function SCH2003 The TOS motif mediates raptor binding and controls multisite 4E-BP1 phosphorylation by mTORC1. |
Co-authors in the Atlas
People with a profile here who share at least one study with Diane C. Fingar.
- John Blenis 3 shared studies Showed early on that rapamycin blocks S6 kinase, then worked out how mTORC1 drives cell growth through its two main translation targets, S6K1 and 4E-BP1. His lab also found, in parallel with the Sabatini lab, that mTORC1 phosphorylates Grb10, a feedback brake on insulin signalling
- Andrew R. Tee First author of one of several 2003 papers showing that the TSC1–TSC2 complex acts as a GTPase-activating protein for Rheb
- Brendan D. Manning 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.
- David M. Sabatini Identified mTOR (as RAFT1) in 1994. His lab then mapped much of the machinery around it: raptor and rictor at the core of mTORC1 and mTORC2, the Rag–Ragulator system that docks mTORC1 on the lysosome, and the sensors that detect leucine, arginine and SAM
- Lewis C. Cantley Co-discovered PI3K, the pathway that feeds into mTOR from growth factors
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