Pathway link ERK-NUCL
ERK / RSK (MAPK) Nucleotide synthesis
ERK / RSK (MAPK) activates Nucleotide synthesis.
ERK2 switches on an enzyme that makes purines.
The conditions it holds under
Human cancer cell lines and xenograft tumours; ERK2, not ERK1; post-translational and parallel to mTORC1. Single study.
- Time it takes
- minutes
- Step
- direct (one molecule acts on the other)
- Measured in
- human cells, mouse xenograft
- Where in the cell
- cytosol
- Reaches people?
- plausible in people, not shown directly
- How settled
- emerging, few independent studies
Studies behind it
| Year | Evidence | Study |
|---|---|---|
| 2020 | M | ERK2 phosphorylates PFAS to mediate posttranslational control of de novo purine synthesisALI2020 The Atlas records several routes by which mTORC1 drives purine synthesis. This study shows mTORC1 is not the only growth pathway with that power: RAS-ERK signalling stimulates purine synthesis directly and within minutes, because ERK2 - but not ERK1 - phosphorylates the purine synthesis enzyme PFAS at Thr619. Cells expressing a PFAS that cannot be phosphorylated make fewer purines, form fewer colonies and grow smaller tumors. Two points bound the mTOR claim: the control is posttranslational, so it acts far faster than transcription or translation, and it is a parallel input, so purine synthesis in a RAS-driven tumor is not read out from mTORC1 activity alone. |
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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