Component
mcm5Um34
The ribose-methylated U34 state in the correction ledger.
3 recorded relationships. Experimental role, claim status and evidence remain attached to each record.
How nutrients influence it
Every nutrient with a recorded effect on this component, credited to the nutrient that acted rather than the chapter that recorded it. Open a nutrient to see the findings and the conditions they were measured under.
Other things that act on it
Enzymes, hormones, genes, and other components with a recorded effect. These are not nutrients, so they do not count toward the arrows above. Each finding names the chapter that recorded it.
How nutrients reach it in more than one step
Chains of two or more recorded steps that end here, grouped by the nutrient they start from. Each step is a separate finding, so a chain is a route a mechanism could take, not proof that it does.
Tracing routes…
What it does
Every recorded relationship this component is part of, grouped by its role. Plain wording comes first; the technical statement follows.
What it acts on
The correction assigns mcm5Um34 to the stress-related selenoprotein set.
Experimental context and source evidence
Selenium corrections and deep dive · lines 1–8
Selenium correction and deep-dive draft · supports · Source draft; model details require primary-source verification · source_derived_draft · unverified_draft
# Correction first In my last message I labeled the tRNA isoforms backwards. Fixing it, because this one matters: - **mcm⁵U34** (no ribose methyl) → supports **housekeeping** selenoproteins: TXNRD1, GPX4 - **mcm⁵Um34** (ribose methylated) → **required** for the **stress-related** set: GPX1, SELENOW The hierarchy table was right. The labels on the two isoforms were flipped. Um34 is the *added* mark, and it's the one you lose first — which is why the proteins that depend on it die first.
Complete structured claim and evidenceSec-tRNA Um34 modification contributes to efficient expression of selected stress-responsive selenoproteins including GPX1.
Experimental context and source evidence
- cell_type
- Mouse tissues and human melanoma cells
- experimental_model
- Transgenic mouse tRNA replacement; mutant affects i6A37 as well as Um34; Biochemistry, human melanoma cells and mouse metastasis/xenograft models
- limitations
- Older tRNA mutant also affects i6A37; no universal exclusive stress/housekeeping routing.
- organism
- Mus musculus and Homo sapiens
Selenium: literature corrections and mechanism additions · lines 1178–1189
Metabolic Ledger literature curation, 17 September 2026; primary papers linked individually · supports · Transgenic mouse tRNA replacement; mutant affects i6A37 as well as Um34; Biochemistry, human melanoma cells and mouse metastasis/xenograft models · secondary_verified · secondary_verified
## um34-selective This tRNA modification helps make some selenium proteins more than others. Sec-tRNA Um34 modification contributes to efficient expression of selected stress-responsive selenoproteins including GPX1. Organism: Mus musculus and Homo sapiens Cell type: Mouse tissues and human melanoma cells Experimental model: Transgenic mouse tRNA replacement; mutant affects i6A37 as well as Um34; Biochemistry, human melanoma cells and mouse metastasis/xenograft models Limitations: Older tRNA mutant also affects i6A37; no universal exclusive stress/housekeeping routing. Primary reference: [Selective rescue of selenoprotein expression in mice lacking a highly specialized methyl group in selenocysteine tRNA](https://digitalcommons.unl.edu/biochemgladyshev/54/) Primary reference: [Selenocysteine tRNA methylation promotes oxidative stress resistance in melanoma metastasis](https://www.nature.com/articles/s43018-024-00844-8)
Complete structured claim and evidence
What acts on it
FTSJ1 catalyzes Sec-tRNA U34 ribose methylation producing the Um34-containing form.
Experimental context and source evidence
- cell_type
- Melanoma cells and biochemical systems
- experimental_model
- Biochemistry, human melanoma cells and mouse metastasis/xenograft models
- limitations
- FTSJ1 deletion is not ordinary dietary selenium deficiency.
- organism
- Homo sapiens
Selenium: literature corrections and mechanism additions · lines 1191–1201
Metabolic Ledger literature curation, 17 September 2026; primary papers linked individually · supports · Biochemistry, human melanoma cells and mouse metastasis/xenograft models · secondary_verified · secondary_verified
## ftsj1-um34 FTSJ1 is the enzyme for the formerly unassigned methylation step. FTSJ1 catalyzes Sec-tRNA U34 ribose methylation producing the Um34-containing form. Organism: Homo sapiens Cell type: Melanoma cells and biochemical systems Experimental model: Biochemistry, human melanoma cells and mouse metastasis/xenograft models Limitations: FTSJ1 deletion is not ordinary dietary selenium deficiency. Primary reference: [Selenocysteine tRNA methylation promotes oxidative stress resistance in melanoma metastasis](https://www.nature.com/articles/s43018-024-00844-8)
Complete structured claim and evidence
The events it takes part in
A mechanism often involves more than two components. These are the full events, with every participant and its role.
Situations it appears in
Low-supply and faulty-machinery situations recorded in the chapters where this component plays a part.
In the sources
Preserved passages that mention this component, quoted exactly. Open one to read it in context.
Open hypotheses
Proposed ideas that involve this component. They are labeled as hypotheses and do not change any recorded statement.
This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.