Component
Mouse Mthfd1 protein
Mus musculus trifunctional Mthfd1 protein.
1 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
Dietary folate depletion increased nuclear Mthfd1 more than twofold in mouse liver at the expense of cytosolic levels.
Experimental context and source evidence
- availability_state
- nutrient_deficiency Imported condition classification; unverified.
- experimental_model
- Dietary depletion and liver fractionation
- exposure
- Assay conditions described in the linked primary study.
- limitations
- Nuclear protection is conditional; it does not prove indefinite resistance to deficiency.
- nutrient_topic
- Folate and folic acid research collection; topical membership is not evidence of a direct dietary effect. · Folate (vitamin B9)
- organism
- Mus musculus
- plain_language
- The enzyme redistributed toward the nucleus as folate supply fell.
- primary_references
- [field-2014] Nuclear enrichment of folate cofactors and methylenetetrahydrofolate dehydrogenase 1 (MTHFD1) protect de novo thymidylate biosynthesis during folate deficiency (2014). https://pubmed.ncbi.nlm.nih.gov/25213861/ DOI: 10.1074/jbc.m114.599589
- tissue_or_cell_type
- Liver
- trigger_kind
- nutrient_deficiency Imported condition classification; unverified.
Folate and folic acid: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 961–971
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Dietary depletion and liver fractionation · source_derived_draft · unverified_draft
### mouse-folate-depletion-mthfd1-enrichment Dietary folate depletion increased nuclear Mthfd1 more than twofold in mouse liver at the expense of cytosolic levels. Condition category: nutrient_deficiency nutrient_topic: Folate and folic acid research collection; topical membership is not evidence of a direct dietary effect. plain_language: The enzyme redistributed toward the nucleus as folate supply fell. organism: Mus musculus tissue_or_cell_type: Liver experimental_model: Dietary depletion and liver fractionation limitations: Nuclear protection is conditional; it does not prove indefinite resistance to deficiency. exposure: Assay conditions described in the linked primary study. [field-2014] Nuclear enrichment of folate cofactors and methylenetetrahydrofolate dehydrogenase 1 (MTHFD1) protect de novo thymidylate biosynthesis during folate deficiency (2014). https://pubmed.ncbi.nlm.nih.gov/25213861/ DOI: 10.1074/jbc.m114.599589
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.