Component
OGT
Enzyme transferring O-linked N-acetylglucosamine to protein substrates.
4 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 acts on it
SELENOV physically associated with OGT in the reported interaction assays.
Experimental context and source evidence
- cell_type
- HEK293T assay system
- experimental_model
- Protein-interaction experiments
- limitations
- Binding does not establish a catalytic substrate relationship.
- organism
- mammalian proteins
Selenium: literature corrections and mechanism additions · lines 810–820
Metabolic Ledger literature curation, 17 September 2026; primary papers linked individually · supports · Protein-interaction experiments · secondary_verified · secondary_verified
## selenov-binds-ogt SELENOV was found to interact with the sugar-transfer enzyme OGT. SELENOV physically associated with OGT in the reported interaction assays. Organism: mammalian proteins Cell type: HEK293T assay system Experimental model: Protein-interaction experiments Limitations: Binding does not establish a catalytic substrate relationship. Primary reference: [Loss of Selenov predisposes mice to extra fat accumulation and attenuated energy expenditure](https://pubmed.ncbi.nlm.nih.gov/34167027/)
Complete structured claim and evidenceSelenov loss reduced adipose OGT protein abundance in mice.
Experimental context and source evidence
- cell_type
- adipose tissue
- experimental_model
- Selenov knockout
- limitations
- Do not equate this perturbation with human dietary deficiency.
- organism
- mouse
Selenium: literature corrections and mechanism additions · lines 834–844
Metabolic Ledger literature curation, 17 September 2026; primary papers linked individually · supports · Selenov knockout · secondary_verified · secondary_verified
## selenov-loss-reduces-ogt-abundance Mouse fat tissue contained less OGT protein after SELENOV loss. Selenov loss reduced adipose OGT protein abundance in mice. Organism: mouse Cell type: adipose tissue Experimental model: Selenov knockout Limitations: Do not equate this perturbation with human dietary deficiency. Primary reference: [Loss of Selenov predisposes mice to extra fat accumulation and attenuated energy expenditure](https://pubmed.ncbi.nlm.nih.gov/34167027/)
Complete structured claim and evidenceSelenov loss reduced adipose OGT activity in mice.
Experimental context and source evidence
- cell_type
- adipose tissue
- experimental_model
- Selenov knockout
- limitations
- Do not equate this perturbation with human dietary deficiency.
- organism
- mouse
Selenium: literature corrections and mechanism additions · lines 822–832
Metabolic Ledger literature curation, 17 September 2026; primary papers linked individually · supports · Selenov knockout · secondary_verified · secondary_verified
## selenov-loss-reduces-ogt-activity Mouse fat tissue had less OGT activity after SELENOV loss. Selenov loss reduced adipose OGT activity in mice. Organism: mouse Cell type: adipose tissue Experimental model: Selenov knockout Limitations: Do not equate this perturbation with human dietary deficiency. Primary reference: [Loss of Selenov predisposes mice to extra fat accumulation and attenuated energy expenditure](https://pubmed.ncbi.nlm.nih.gov/34167027/)
Complete structured claim and evidence
Where it participates (unsigned role)
Selenov loss reduced measured protein O-GlcNAcylation in adipose tissue.
Experimental context and source evidence
- cell_type
- adipose tissue
- experimental_model
- Selenov knockout
- limitations
- The extended AMPK pathway remains partly proposed.
- organism
- mouse
Selenium: literature corrections and mechanism additions · lines 846–856
Metabolic Ledger literature curation, 17 September 2026; primary papers linked individually · supports · Selenov knockout · secondary_verified · secondary_verified
## selenov-loss-reduces-o-glcnacylation Protein sugar modification fell after SELENOV loss in this model. Selenov loss reduced measured protein O-GlcNAcylation in adipose tissue. Organism: mouse Cell type: adipose tissue Experimental model: Selenov knockout Limitations: The extended AMPK pathway remains partly proposed. Primary reference: [Loss of Selenov predisposes mice to extra fat accumulation and attenuated energy expenditure](https://pubmed.ncbi.nlm.nih.gov/34167027/)
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.