Pathway link MTORC1-SAM
mTORC1 S-adenosylmethionine (SAM)
mTORC1 activates S-adenosylmethionine (SAM).
mTORC1 tells the cell to make more SAM.
The conditions it holds under
Human cell lines and mouse xenograft tumours; acts through c-MYC on MAT2A. Together with SAM-SAMTOR this forms a loop whose behaviour in normal tissue is untested. Single study.
- Time it takes
- hours
- Step
- indirect (through steps not drawn here)
- Measured in
- human cells, mouse xenograft
- Where in the cell
- nucleus
- Reaches people?
- plausible in people, not shown directly
- How settled
- emerging, few independent studies
Studies behind it
| Year | Evidence | Study |
|---|---|---|
| 2021 | M | mTORC1 stimulates cell growth through SAM synthesis and m6A mRNA-dependent control of protein synthesisVIL2021 SAMTOR (GU2017) showed the cell can sense S-adenosylmethionine and report it to mTORC1. This study runs the arrow the other way: mTORC1 controls how much SAM the cell makes. Downstream of mTORC1, c-MYC binds intron 1 of MAT2A and raises expression of the enzyme that produces SAM, the cell's main methyl donor; mTORC1 separately increases the protein level of WTAP, the regulatory subunit of the m6A RNA methyltransferase complex. Together these raise m6A methylation of mRNA, which primes the translation machinery for growth. Blocking MAT2A lowers SAM, m6A, protein synthesis rate and tumor growth. |
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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