Targets for cell cycle arrest by the immunosuppressant rapamycin in yeast
What this study shows
Discovery of the TOR1 and TOR2 genes in yeast as the targets whose disruption causes rapamycin's cell-cycle-arresting toxicity - the original genetic identification of the TOR pathway.
At a glance
| Evidence type | M Molecular — cells, biochemistry, structure Marked M because it is molecular or in-vitro work (model: Yeast (Saccharomyces cerevisiae)) rather than a whole-organism health-outcome study. That is often exactly where causal biology gets established -- the code says which system the finding was shown in, and nothing about how good the work is. |
| Study type | 5 - Mechanistic / In Vitro |
| Model system | Yeast (Saccharomyces cerevisiae) |
| Journal | Science |
| Year | 1991 |
| Peer reviewed | Yes |
| Record last updated | 2026-10-01 |
| Source | DOI 10.1126/science.1715094 · PMID 1715094 |
Extracted findings
These fields were extracted from the paper with AI assistance and have not been checked against the source. Read them as a pointer into the paper, not as curated claims; where they disagree with the curated summary above, the curated summary stands.
| Intervention | Rapamycin (FKBP-rapamycin); genetic (FPR1, TOR) |
| Target | FKBP / TOR |
| Model | Yeast (S. cerevisiae) |
| Effect | FKBP-rapamycin complex arrests cells in G1; identified FKBP and TOR as targets – a foundational discovery |
In the Atlas
Related topics
Open questions that cite this study
- Cited as supporting evidence for the open question Is there a low-dose mTOR schedule whose immune effects come out favourable, compartment by compartment?.
Answers that reference this study
- Discussed in the plain-language answer What is mTOR?.
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