Pathway link MTORC1-ROS
mTORC1 Reactive oxygen species
mTORC1 activates Reactive oxygen species.
Switching mTORC1 on too much pushes resting stem cells to start dividing and floods them with reactive, damaging molecules; giving them antioxidants restores their normal function.
The conditions it holds under
Demonstrated in haematopoietic stem cells, where quiescence is the baseline state. Cell types that are already cycling need not behave this way.
- Time it takes
- days
- Step
- indirect (through steps not drawn here)
- Measured in
- mouse
- Where in the cell
- mitochondrion
- Reaches people?
- plausible in people, not shown directly
- How settled
- emerging, few independent studies
Studies behind it
| Year | Evidence | Study |
|---|---|---|
| 2008 | A | TSC-mTOR maintains quiescence and function of hematopoietic stem cells by repressing mitochondrial biogenesis and reactive oxygen speciesCHE2008 Showed why blood stem cells must keep mTOR LOW. Deleting TSC1 (which unleashes mTOR) drove resting stem cells into rapid division, flooded them with reactive oxygen species, and burned out their ability to self-renew. An antioxidant rescued them. A key link between mTOR, stem-cell exhaustion, and tissue aging. |
Points the other way
No study in the Atlas contradicts this link. That means none in this curated set, not none in the literature.
Who has checked this
- Checked by
- No researcher outside the project has checked this link yet.
- Curator sign-off
- Not signed off yet. This link was drafted with AI help and has not been reviewed link by link; treat it as a proposal until it is.
- Curated by
- Oliver Barton, with AI help for drafting; see how links are checked.
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