S6K1- and betaTRCP-mediated degradation of PDCD4 promotes protein translation and cell growth
What this study shows
S6K1 triggers betaTRCP-mediated degradation of the tumour suppressor PDCD4 to promote translation.
At a glance
| Evidence type | M Molecular — cells, biochemistry, structure Marked M because it is molecular or in-vitro work (model: Mammalian cells) 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 | Mammalian cells |
| Journal | Science |
| Year | 2006 |
| Peer reviewed | Yes |
| Record last updated | 2026-10-01 |
| Source | DOI 10.1126/science.1130276 · PMID 17053147 |
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 | Biochemical/genetic (S6K1, βTRCP, PDCD4) |
| Target | S6K1 / PDCD4 / eIF4A |
| Model | Mammalian cells |
| Effect | S6K1 phosphorylates PDCD4 (Ser67) triggering βTRCP-mediated degradation → promotes translation and cell growth |
In the Atlas
Related topics
Links in the pathway map
- Supports S6K1 inhibits PDCD4
More studies on this topic
- Pdcd4-Rictor interaction suppresses mTORC2-PFKFB3 axis and tumorigenesis in NSCLC. (2026)
- Lifespan extension by conditions that inhibit translation in Caenorhabditis elegans (2007)
- The Circadian Protein BMAL1 Regulates Translation in Response to S6K1-Mediated Phosphorylation (2015)
- Akt/mTOR pathway is a crucial regulator of skeletal muscle hypertrophy and can prevent muscle atrophy in vivo (2001)
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