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[Biochemistry](https://durgical.com/en/biochemistry/) · Enzyme

# mTOR (mechanistic target of rapamycin)

A kinase that decides whether the cell grows: with enough nutrients, insulin and energy it switches on protein synthesis and stops autophagy.

Updated 2026-11-01

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## Key facts

- It forms two complexes: mTORC1 (with raptor, rapamycin-sensitive) and mTORC2 (with rictor, activates Akt).
- mTORC1 integrates amino acids (Rag GTPases on the lysosome), insulin/growth factors (Akt → TSC2 → Rheb) and energy (AMPK holds it back).
- It activates S6K1 and inhibits 4E-BP1: more protein translation; it also switches on lipid synthesis (SREBP) and stops autophagy (ULK1).
- Structure 4JSV is human mTOR (catalytic region) with mLST8, ADP and Mg²⁺ in the active site.

**Also called**
mTORC1, mTORC2

**EC number**
[2.7.11.1](https://www.enzyme-database.org/query.php?ec=2.7.11.1)

**Genes**
MTOR

**Structure (PDB)**
[4JSV](https://www.rcsb.org/structure/4JSV)

## Regulation

- Activation: amino acids (especially leucine), insulin and IGF-1 through Akt, Rheb-GTP.
- Inhibition: the TSC1/TSC2 complex, AMPK (low energy), hypoxia, lack of amino acids.
- S6K1 phosphorylates IRS-1 and dampens insulin signalling (negative feedback).

## Inhibitors and toxins

- Rapamycin (sirolimus) bound to FKBP12, everolimus, temsirolimus
- ATP-competitive inhibitors (research use)

## Clinical notes

- Tuberous sclerosis: loss of TSC1 or TSC2 leaves mTORC1 on and causes benign tumours in brain, skin, kidney and heart; mTOR inhibitors shrink some of them.
- Sirolimus and everolimus are used as immunosuppressants in transplants and in some cancers.
- Chronic activation of mTORC1 and S6K1 by nutrient excess contributes to insulin resistance.

## Related conditions

- [Breast cancer](https://durgical.com/en/conditions/breast-cancer/)
- [Type 2 diabetes mellitus](https://durgical.com/en/conditions/type-2-diabetes-mellitus/)

## Related

- [AMP-activated protein kinase (AMPK)](https://durgical.com/en/biochemistry/enzymes/amp-activated-protein-kinase/)
- [Insulin signalling](https://durgical.com/en/biochemistry/topics/insulin-signalling/)
- [Receptor tyrosine kinases](https://durgical.com/en/biochemistry/topics/receptor-tyrosine-kinases/)
- [Insulin receptor](https://durgical.com/en/biochemistry/enzymes/insulin-receptor/)
- [Fed, fasting and starvation states](https://durgical.com/en/biochemistry/topics/fed-fasting-and-starvation-states/)
- [Leptin, appetite and obesity](https://durgical.com/en/biochemistry/topics/leptin-appetite-and-obesity/)

## Test yourself

Think of the answer, then tap the question to see it.

## Which three signals does mTORC1 integrate to decide on cell growth?

Amino acids, insulin or growth factors, and energy status (through AMPK).

## How does rapamycin work?

It binds FKBP12 and the complex blocks mTORC1.

## Which disease does loss of the TSC1/TSC2 complex cause?

Tuberous sclerosis, from excessive mTORC1 activity.

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Educational information, not medical advice. For any symptom, see a health professional.

Sources: [MTOR: Serine/threonine-protein kinase mTOR (human)](https://www.uniprot.org/uniprotkb/P42345/entry) (UniProt, 2026); [4JSV: mTOR kinase structure, mechanism and regulation.](https://www.rcsb.org/structure/4JSV) (RCSB Protein Data Bank, 2026); [MTOR gene: MedlinePlus Genetics](https://medlineplus.gov/genetics/gene/mtor/) (MedlinePlus, US National Library of Medicine, 2026); [Tuberous sclerosis complex: MedlinePlus Genetics](https://medlineplus.gov/genetics/condition/tuberous-sclerosis-complex/) (MedlinePlus, US National Library of Medicine, 2026); Textbook of Biochemistry for Medical Students, 6th ed. (Jaypee Brothers Medical Publishers (Vasudevan DM, Sreekumari S, Vaidyanathan K), 2011).

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Representative model, for educational purposes only.

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