5'TOP mRNA
Class of mRNAs with a 5' terminal oligopyrimidine tract encoding ribosomal proteins and translation factors; their translation is a canonical output of mTORC1 signaling.
The messages that build the factory parts. A group of messenger RNAs (the templates cells read to build proteins) that mostly encode the protein-building machinery itself. Turning their translation on is one of mTORC1's classic, best-established jobs.
Ribosome profiling showed the mTORC1 response here is transcript-selective rather than uniform, which is why 'mTORC1 increases protein synthesis' is a summary that hides the actual biology: the output is transcript choice.
TL;DR. 5'TOP mRNA appears in 3 curated studies in Oliver's mTOR Atlas: 1 in animal models; 2 at the molecular level (cells, biochemistry, structure). No study in people is recorded for it in the Atlas yet. It has 1 interaction in the curated pathway model.
In the pathway model
| Interaction | Mechanism | Evidence | Studies |
|---|---|---|---|
| mTORC1 activates 5'TOP mRNA mechanism: functional-consequence · this link in full · on the map table | When mTORC1 is on, the cell does not simply make more of every protein. It preferentially makes the parts of its own protein-making machinery, from a particular class of messages marked at one end. mTORC1 raises translation of the 5'TOP class of mRNAs, which encode ribosomal proteins and translation factors. Ribosome profiling showed the effect is selective rather than uniform: mTORC1 does not turn all translation up equally, it shifts which transcripts get translated. mTORC1 raises translation of the 5'TOP class of mRNAs, which encode ribosomal proteins and translation factors. Ribosome profiling showed the effect is selective rather than uniform: mTORC1 does not turn all translation up equally, it shifts which transcripts get translated. Holds under: The selectivity is from ribosome profiling in cancer cell lines (HSI2012); the lifespan link is Drosophila only (WAN2026); PLEDGER2026 shows the same arm being repressed in chronically activated human CD8+ T cells. No human in vivo measurement of 5'TOP translation under an mTOR inhibitor in this corpus. Which of the 5'TOP transcripts matter for which phenotype is not resolved. plausible in people, not shown directly · settled in the literature | A | HSI2012, WAN2026, PLEDGER2026 |
Evidence at a glance
| Evidence | What it means | Studies |
|---|---|---|
| A | Animal model | 1 |
| M | Molecular — cells, biochemistry, structure | 2 |
No direct human evidence in the Atlas for this entity yet — everything below rests on animal or molecular work.
Studies
| Year | Evidence | Study |
|---|---|---|
| 2026 | A | Lsp2 links mTORC1 to TOP mRNA translation and lifespan in Drosophila WAN2026 Identifies Lsp2, a Drosophila fat-body storage protein, as an amino-acid-induced feedback activator of mTORC1 that specifically boosts translation of TOP-motif mRNAs (mostly ribosomal proteins) via 4E-BP — a rapamycin-resistant arm of mTORC1 output. Genetic loss of Lsp2 reduces TOP mRNA translation and robustly extends lifespan without cost to reproduction, revealing a rapamycin-independent route from mTORC1 activity to organismal longevity. |
| 2026 | M | Translational repression of 5' TOP mRNAs in chronically activated CD8+ T cells in vitro. PLEDGER2026 Ribosome profiling of exhausted human CD8+ T cells reveals marked repression of 5'TOP mRNAs despite elevated mTOR activity, uncovering a layer of translational control that overrides or bypasses mTOR in T cell exhaustion. |
| 2026 | M | mTOR inactivation governs adaptive survival to ribosome biogenesis deficiency FAN2026 mTORC1 inhibition does not restore ribosome biogenesis but redistributes limited ribosomes away from highly-translated 5'TOP mRNAs toward survival-essential transcripts, defining a 'translational fitness' mechanism that lets cancer cells survive ribosome biogenesis deficiency. |
Related entities
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