Rapamycin-FKBP specifically blocks growth-dependent activation of and signaling by the 70 kd S6 protein kinases
What this study shows
Rapamycin-FKBP12 complex blocks growth-factor activation of p70 S6 kinase, linking the drug to a specific mitogenic pathway.
At a glance
| Evidence type | M Molecular — cells, biochemistry, structure Marked M because it is molecular or in-vitro work (model: T cells; in vitro) 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 | T cells; in vitro |
| Journal | Cell |
| Year | 1992 |
| Peer reviewed | Yes |
| Record last updated | 2026-10-01 |
| Source | DOI 10.1016/0092-8674(92)90643-q · PMID 1377606 |
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 (± FK506) |
| Target | FKBP / p70 S6 kinase |
| Model | T cells; in vitro |
| Effect | Rapamycin blocks activation of the p70 S6 kinases; FK506 reverses it (FKBP-dependent) |
In the Atlas
Links in the pathway map
- Supports FKBP12 binds mTORC1
- Supports mTORC1 activates S6K1
- Supports Rapamycin inhibits mTORC1
Learn the biology
Want to understand the biology behind this study? → Challenge 02: Why rapamycin does not switch mTORC1 off
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