What is mTOR?
mTOR (mechanistic target of rapamycin, also written FRAP1 in older literature) is a serine/threonine protein kinase – an enzyme that turns other proteins on or off by adding phosphate groups to them. It sits at the center of how a cell decides whether to grow: when nutrients, growth factors, and energy are abundant, mTOR is active and pushes the cell to build proteins and grow; when any of those are scarce, mTOR switches off and the cell shifts to conserving and recycling resources instead.
Named after the drug that found it, not the other way around
mTOR wasn't discovered by studying growth signaling directly – it was found because of a drug.
- VEZ1975 M – rapamycin was first isolated in 1975 from Streptomyces hygroscopicus, a bacterium in a soil sample from Rapa Nui (Easter Island) – originally studied as an antifungal antibiotic, years before anyone knew what it did to cells.
- HEI1991 M – geneticists studying why yeast cells resist growth-arrest by the immunosuppressant rapamycin found the genes responsible – TOR1 and TOR2 ("target of rapamycin") – giving the pathway its name before the human version was even known.
- PRI1992 M – showed rapamycin inhibits the 70-kilodalton S6 kinase, identifying one of the first known downstream targets of the then-unnamed pathway in mammalian cells.
The mammalian version of TOR – what we now call mTOR – was cloned by three independent labs in 1994, using rapamycin itself as the molecular hook to fish it out.
What mTOR actually does
mTOR works as the catalytic core of two distinct protein complexes with different jobs – mTORC1 and mTORC2, covered in full on their own answer page. In short: mTORC1 is the nutrient/growth-factor sensor that controls protein synthesis, autophagy, and growth – and is rapamycin's direct target. mTORC2 is involved in cell survival and glucose metabolism, and is only reached by rapamycin indirectly, with chronic dosing.
Why it matters beyond basic biology
Because mTOR sits at the intersection of nutrient sensing, growth, and metabolism, its dysregulation shows up across an unusually wide range of conditions: cancer (see how mTOR connects to cancer), the genetic disorder tuberous sclerosis complex (where a mutation leaves mTORC1 switched on without its growth-factor brake), and the biology of aging, where inhibiting it with rapamycin is the most consistent drug-based way known to extend lifespan in laboratory animals across species.
Related entities
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