Component
De novo purine nucleotide synthesis
Defined biochemical process or measured endpoint; not a unique causal entity for an entire sentence.
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 acts on it
Formate incorporation through de novo purine synthesis was not significantly altered in these MTHFD1-deficient fibroblasts.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- experimental_model
- Formate suppression assay
- exposure
- Assay conditions described in the linked primary study.
- limitations
- Preservation in this genotype does not establish dispensability of MTHFD1.
- nutrient_topic
- Folate and folic acid research collection; topical membership is not evidence of a direct dietary effect. · Folate (vitamin B9)
- organism
- Homo sapiens
- plain_language
- Different folate-dependent pathways were not equally impaired.
- primary_references
- [field-2015] Human mutations in methylenetetrahydrofolate dehydrogenase 1 impair nuclear de novo thymidylate biosynthesis (2015). https://pubmed.ncbi.nlm.nih.gov/25548164/ DOI: 10.1073/pnas.1414555112
- tissue_or_cell_type
- WG3607 fibroblasts
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Folate and folic acid: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1194–1204
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Formate suppression assay · source_derived_draft · unverified_draft
### mthfd1-patient-purine-preservation Formate incorporation through de novo purine synthesis was not significantly altered in these MTHFD1-deficient fibroblasts. Condition category: machinery_impairment nutrient_topic: Folate and folic acid research collection; topical membership is not evidence of a direct dietary effect. plain_language: Different folate-dependent pathways were not equally impaired. organism: Homo sapiens tissue_or_cell_type: WG3607 fibroblasts experimental_model: Formate suppression assay limitations: Preservation in this genotype does not establish dispensability of MTHFD1. exposure: Assay conditions described in the linked primary study. [field-2015] Human mutations in methylenetetrahydrofolate dehydrogenase 1 impair nuclear de novo thymidylate biosynthesis (2015). https://pubmed.ncbi.nlm.nih.gov/25548164/ DOI: 10.1073/pnas.1414555112
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.