Component
FTSJ1
tRNA methyltransferase identified as the tRNA[Ser]Sec Um34 methyltransferase in 2024.
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
Experimental FTSJ1 loss reduces efficient selenocysteine insertion at UGA.
Experimental context and source evidence
- availability_state
- Experimental loss of FTSJ1-dependent tRNA modification.
- experimental_scope
- Cell/biochemical studies and melanoma xenograft models reported in the 2024 FTSJ1 study.
- limitations
- FTSJ1 loss is a machinery perturbation, not itself a nutritional selenium-deficiency syndrome. The results do not prove that Um34 determines every selenoprotein phenotype.
- trigger_kind
- machinery_impairment
Selenium deficiency: a mechanism-first reference · lines 75–75
Supplied selenium deficiency reference · supports · Supplied reference; verify the primary study and experimental context. · source_derived_draft · unverified_draft
Update: FTSJ1 was identified in 2024 as the tRNA^[Ser]Sec Um34 methyltransferase. Loss of FTSJ1 reduced efficient Sec insertion and sensitized experimental cells to oxidative stress. Evidence: cell/biochemical and melanoma xenograft models. [1]
Complete structured claim and evidenceExperimental cells lacking FTSJ1 become more sensitive to oxidative stress.
Experimental context and source evidence
- availability_state
- Experimental loss of FTSJ1-dependent tRNA modification.
- experimental_scope
- Cell/biochemical studies and melanoma xenograft models reported in the 2024 FTSJ1 study.
- limitations
- FTSJ1 loss is a machinery perturbation, not itself a nutritional selenium-deficiency syndrome. The results do not prove that Um34 determines every selenoprotein phenotype.
- trigger_kind
- machinery_impairment
Selenium deficiency: a mechanism-first reference · lines 75–75
Supplied selenium deficiency reference · supports · Supplied reference; verify the primary study and experimental context. · source_derived_draft · unverified_draft
Update: FTSJ1 was identified in 2024 as the tRNA^[Ser]Sec Um34 methyltransferase. Loss of FTSJ1 reduced efficient Sec insertion and sensitized experimental cells to oxidative stress. Evidence: cell/biochemical and melanoma xenograft models. [1]
Complete structured claim and evidenceFTSJ1 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.