Component
Human choline acetyltransferase / CHAT
Human choline acetyltransferase / CHAT. Species, exposure and limitations are retained in each linked 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
ChAT catalyzes reversible acetylcholine synthesis from choline and acetyl-CoA.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/choline-research/11172068.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "691b96b9c5c149c554b99d8e1532ffee25084a8970f8deb23f0991dfd6013d39", "start_char": 0, "end_char": 1231, "text_sha256": "691b96b9c5c149c554b99d8e1532ffee25084a8970f8deb23f0991dfd6013d39"}
- experimental_model
- Human CHAT genetics, recombinant expression and enzyme kinetics
- exposure
- Ten recessive variants in five patients; nine mutant proteins assayed
- limitations
- Inherited enzyme defects, not a dietary choline-deficiency model. Acetyl-CoA and choline are distinct substrates.
- nutrient_topic
- Choline research collection; topical membership is not evidence of a direct dietary effect. · Choline
- organism
- Human CHAT proteins; COS-cell and bacterial expression systems
- plain_language
- The neurotransmitter needs both the choline headgroup and an acetyl group supplied by acetyl-CoA.
- primary_references
- [choline-p11172068] Choline acetyltransferase mutations cause myasthenic syndrome associated with episodic apnea in humans. (2001). https://pubmed.ncbi.nlm.nih.gov/11172068/ DOI: 10.1073/pnas.98.4.2017
- tissue_or_cell_type
- Neuromuscular acetylcholine resynthesis
Choline: metabolism, signaling and nutrient connections (2026-09-17) · lines 412–423
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human CHAT genetics, recombinant expression and enzyme kinetics · source_derived_draft · unverified_draft
### choline-chat-acetylcholine ChAT catalyzes reversible acetylcholine synthesis from choline and acetyl-CoA. Condition category: normal nutrient_topic: Choline research collection; topical membership is not evidence of a direct dietary effect. plain_language: The neurotransmitter needs both the choline headgroup and an acetyl group supplied by acetyl-CoA. organism: Human CHAT proteins; COS-cell and bacterial expression systems tissue_or_cell_type: Neuromuscular acetylcholine resynthesis experimental_model: Human CHAT genetics, recombinant expression and enzyme kinetics limitations: Inherited enzyme defects, not a dietary choline-deficiency model. Acetyl-CoA and choline are distinct substrates. exposure: Ten recessive variants in five patients; nine mutant proteins assayed evidence_span: {"source_cache": "artifacts/choline-research/11172068.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "691b96b9c5c149c554b99d8e1532ffee25084a8970f8deb23f0991dfd6013d39", "start_char": 0, "end_char": 1231, "text_sha256": "691b96b9c5c149c554b99d8e1532ffee25084a8970f8deb23f0991dfd6013d39"} [choline-p11172068] Choline acetyltransferase mutations cause myasthenic syndrome associated with episodic apnea in humans. (2001). https://pubmed.ncbi.nlm.nih.gov/11172068/ DOI: 10.1073/pnas.98.4.2017
Complete structured claim and evidence
Where it participates (unsigned role)
Bacterially expressed human ChAT E441K lacked catalytic activity in the reported kinetic experiment.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_span
- {"source_cache": "artifacts/choline-research/11172068.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "691b96b9c5c149c554b99d8e1532ffee25084a8970f8deb23f0991dfd6013d39", "start_char": 0, "end_char": 1231, "text_sha256": "691b96b9c5c149c554b99d8e1532ffee25084a8970f8deb23f0991dfd6013d39"}
- experimental_model
- Human CHAT genetics, recombinant expression and enzyme kinetics
- exposure
- Ten recessive variants in five patients; nine mutant proteins assayed
- limitations
- Inherited enzyme defects, not a dietary choline-deficiency model. Acetyl-CoA and choline are distinct substrates.
- nutrient_topic
- Choline research collection; topical membership is not evidence of a direct dietary effect. · Choline
- organism
- Human CHAT proteins; COS-cell and bacterial expression systems
- plain_language
- Having the nutrient present cannot by itself guarantee synthesis when the enzyme is inactive.
- primary_references
- [choline-p11172068] Choline acetyltransferase mutations cause myasthenic syndrome associated with episodic apnea in humans. (2001). https://pubmed.ncbi.nlm.nih.gov/11172068/ DOI: 10.1073/pnas.98.4.2017
- tissue_or_cell_type
- Neuromuscular acetylcholine resynthesis
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Choline: metabolism, signaling and nutrient connections (2026-09-17) · lines 425–436
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human CHAT genetics, recombinant expression and enzyme kinetics · source_derived_draft · unverified_draft
### choline-chat-e441k Bacterially expressed human ChAT E441K lacked catalytic activity in the reported kinetic experiment. Condition category: machinery_impairment nutrient_topic: Choline research collection; topical membership is not evidence of a direct dietary effect. plain_language: Having the nutrient present cannot by itself guarantee synthesis when the enzyme is inactive. organism: Human CHAT proteins; COS-cell and bacterial expression systems tissue_or_cell_type: Neuromuscular acetylcholine resynthesis experimental_model: Human CHAT genetics, recombinant expression and enzyme kinetics limitations: Inherited enzyme defects, not a dietary choline-deficiency model. Acetyl-CoA and choline are distinct substrates. exposure: Ten recessive variants in five patients; nine mutant proteins assayed evidence_span: {"source_cache": "artifacts/choline-research/11172068.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "691b96b9c5c149c554b99d8e1532ffee25084a8970f8deb23f0991dfd6013d39", "start_char": 0, "end_char": 1231, "text_sha256": "691b96b9c5c149c554b99d8e1532ffee25084a8970f8deb23f0991dfd6013d39"} [choline-p11172068] Choline acetyltransferase mutations cause myasthenic syndrome associated with episodic apnea in humans. (2001). https://pubmed.ncbi.nlm.nih.gov/11172068/ DOI: 10.1073/pnas.98.4.2017
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.