Abstract
The inhibition of the central growth regulatory kinase TOR, which participates in two complexes, TORC1 and TORC2, has been a focus of metabolic and cancer studies for many years. Most studies have dealt with TORC1, the canonical target of rapamycin, and the role of this complex in autophagy, protein synthesis, and cell growth control. Recent work on TORC2 in budding and fission yeast species points to a conserved role of this lesser-known TOR complex in the survival of DNA damage. In budding yeast, TORC2 controls lipid biosynthesis and actin cytoskeleton through downstream AGC kinases, which are now, surprisingly, implicated in the survival of oxidative DNA damage. Preliminary data from mTORC2 modulation in cancer cells suggest that an extension to human chemotherapy is worth exploring.
| Original language | English |
|---|---|
| Pages (from-to) | 995-1002 |
| Number of pages | 8 |
| Journal | EMBO Molecular Medicine |
| Volume | 6 |
| Issue number | 8 |
| DOIs | |
| State | Published - Aug 2014 |
UN SDGs
This output contributes to the following UN Sustainable Development Goals (SDGs)
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SDG 3 Good Health and Well-being
Keywords
- Cancer therapies
- DNA damage
- MTOR
- TORC1
- TORC2
All Science Journal Classification (ASJC) codes
- Molecular Medicine
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