Redox-sensitive mTOR-eIF4A signaling promotes selective P-glycoprotein translation.
What this study shows
Oxidative stress activates a redox-sensitive PI3K-AKT-mTORC1-eIF4A cascade that selectively promotes P-glycoprotein translation via cap-dependent mRNA engagement, revealing a transcription-independent mechanism of rapid multidrug resistance induction.
At a glance
| Evidence type | M Molecular — cells, biochemistry, structure Marked M because it is molecular or in-vitro work (model: Cell line) 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 | Cell line |
| Journal | Free radical biology & medicine |
| Year | 2026 |
| Peer reviewed | Yes |
| Record last updated | 2026-10-01 |
| Source | DOI 10.1016/j.freeradbiomed.2026.07.033 · PMID 42468714 |
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 | Glucosamine; redox stress |
| Target | mTORC1 / eIF4A / 4E-BP1 |
| Model | Cell line |
| Effect | mTOR-eIF4A selectively upregulates P-gp translation under oxidative stress; multidrug resistance |
In the Atlas
Related topics
Links in the pathway map
More studies on this topic
- ATM signals to TSC2 in the cytoplasm to regulate mTORC1 in response to ROS (2010)
- TSC-mTOR maintains quiescence and function of hematopoietic stem cells by repressing mitochondrial biogenesis and reactive oxygen species (2008)
- Redox activation of ATG5 licenses autophagy upon nutrient restriction (2026)
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