Component
Mouse glycine decarboxylase / Gldc
Context-specific entity; species, compartment and exposure are stated on each claim.
2 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
Reducing Gldc expression in mice suppressed glycine cleavage and depleted one-carbon-bearing folates while glycine accumulated.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_access
- Primary full text
- experimental_model
- Mouse gene-trap model; enzyme activity and tissue metabolites.
- limitations
- Inherited processing failure is distinct from insufficient dietary glycine.
- nutrient_topic
- Glycine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Glycine
- plain_language
- Excess glycine can coexist with a shortage of products made from it.
- primary_references
- Glycine decarboxylase deficiency causes neural tube defects and features of non-ketotic hyperglycinemia in mice. · 2015 · https://pubmed.ncbi.nlm.nih.gov/25736695/ · DOI 10.1038/ncomms7388
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Glycine: supply, one-carbon allocation, receptors and cross-nutrient mechanisms (2026-09-19) · lines 130–136
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse gene-trap model; enzyme activity and tissue metabolites. · source_derived_draft · unverified_draft
## glycine-gldc-one-carbon-loss Excess glycine can coexist with a shortage of products made from it. Reducing Gldc expression in mice suppressed glycine cleavage and depleted one-carbon-bearing folates while glycine accumulated. Model: Mouse gene-trap model; enzyme activity and tissue metabolites. Limitations: Inherited processing failure is distinct from insufficient dietary glycine. Evidence access: Primary full text Glycine decarboxylase deficiency causes neural tube defects and features of non-ketotic hyperglycinemia in mice. · 2015 · https://pubmed.ncbi.nlm.nih.gov/25736695/ · DOI 10.1038/ncomms7388
Complete structured claim and evidence
Where it participates (unsigned role)
Formate treatment normalized folate profiles, restored embryonic growth and prevented neural-tube defects in the tested Gldc-deficient mice.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_access
- Primary full text
- experimental_model
- Mouse developmental model and formate supplementation.
- limitations
- Does not establish treatment of human nonketotic hyperglycinemia or prove all disease features are formate-responsive.
- nutrient_topic
- Glycine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Glycine
- plain_language
- A downstream carbon donor bypassed part of the missing pathway.
- primary_references
- Glycine decarboxylase deficiency causes neural tube defects and features of non-ketotic hyperglycinemia in mice. · 2015 · https://pubmed.ncbi.nlm.nih.gov/25736695/ · DOI 10.1038/ncomms7388
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Glycine: supply, one-carbon allocation, receptors and cross-nutrient mechanisms (2026-09-19) · lines 138–144
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse developmental model and formate supplementation. · source_derived_draft · unverified_draft
## glycine-gldc-formate-bypass A downstream carbon donor bypassed part of the missing pathway. Formate treatment normalized folate profiles, restored embryonic growth and prevented neural-tube defects in the tested Gldc-deficient mice. Model: Mouse developmental model and formate supplementation. Limitations: Does not establish treatment of human nonketotic hyperglycinemia or prove all disease features are formate-responsive. Evidence access: Primary full text Glycine decarboxylase deficiency causes neural tube defects and features of non-ketotic hyperglycinemia in mice. · 2015 · https://pubmed.ncbi.nlm.nih.gov/25736695/ · DOI 10.1038/ncomms7388
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.