Component
Chinese hamster HACL1
Cricetulus griseus HACL1 investigated in CHO-K1 knockout cells.
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
Added 2-hydroxypalmitate increased odd-chain phosphatidylcholine in either single Hacl knockout, but not in the Hacl1/Hacl2 double knockout.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence
- [{"paper_key": "kitamura-2017-hacl2", "source_bundle": "artifacts/thiamine_metabolism_sources.json", "passage_ids": ["p-42", "p-53"], "locator": "such an increase was not observed", "preservation": "Exact text retained in the source bundle; full source document retained when openly retrievable."}]
- experimental_model
- CHO-K1 knockout; 2-hydroxypalmitate feeding and LC-MS/MS.
- limitations
- Substrate-specific redundancy; does not establish equal contributions in human tissues.
- nutrient
- Thiamine (vitamin B1) · Thiamine (vitamin B1)
- nutrient_topic
- Thiamine research collection; topical membership is not evidence of a direct dietary effect. · Thiamine (vitamin B1)
- organism
- Cricetulus griseus
- plain_language
- For an externally supplied hydroxy-fatty acid, either lyase could support the measured route; this differs from phytosphingosine-derived substrate routing.
- primary_references
- [kitamura-2017-hacl2] Phytosphingosine degradation pathway includes fatty acid α-oxidation reactions in the endoplasmic reticulum (2017). https://pubmed.ncbi.nlm.nih.gov/28289220/ DOI: 10.1073/pnas.1700138114
- tissue_or_cell_type
- Ovary-derived CHO-K1 cells
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Thiamine: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1057–1068
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · CHO-K1 knockout; 2-hydroxypalmitate feeding and LC-MS/MS. · source_derived_draft · unverified_draft
### b1-hamster-hacl-redundant-free-hydroxyacid Added 2-hydroxypalmitate increased odd-chain phosphatidylcholine in either single Hacl knockout, but not in the Hacl1/Hacl2 double knockout. Condition category: machinery_impairment nutrient_topic: Thiamine research collection; topical membership is not evidence of a direct dietary effect. plain_language: For an externally supplied hydroxy-fatty acid, either lyase could support the measured route; this differs from phytosphingosine-derived substrate routing. organism: Cricetulus griseus tissue_or_cell_type: Ovary-derived CHO-K1 cells experimental_model: CHO-K1 knockout; 2-hydroxypalmitate feeding and LC-MS/MS. limitations: Substrate-specific redundancy; does not establish equal contributions in human tissues. evidence: [{"paper_key": "kitamura-2017-hacl2", "source_bundle": "artifacts/thiamine_metabolism_sources.json", "passage_ids": ["p-42", "p-53"], "locator": "such an increase was not observed", "preservation": "Exact text retained in the source bundle; full source document retained when openly retrievable."}] nutrient: Thiamine (vitamin B1) [kitamura-2017-hacl2] Phytosphingosine degradation pathway includes fatty acid α-oxidation reactions in the endoplasmic reticulum (2017). https://pubmed.ncbi.nlm.nih.gov/28289220/ DOI: 10.1073/pnas.1700138114
Complete structured claim and evidence
Where it participates (unsigned role)
Hacl2 knockout reduced phytosphingosine-derived glycerolipid labeling more strongly than Hacl1 knockout in CHO-K1 cells.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence
- [{"paper_key": "kitamura-2017-hacl2", "source_bundle": "artifacts/thiamine_metabolism_sources.json", "passage_ids": ["p-42", "p-61"], "locator": "higher contribution of HACL2", "preservation": "Exact text retained in the source bundle; full source document retained when openly retrievable."}]
- experimental_model
- CHO-K1 knockout and radiolabeled phytosphingosine tracing.
- limitations
- Genetic cell model; does not establish human tissue dominance or thiamine-deficiency pathology.
- nutrient
- Thiamine (vitamin B1) · Thiamine (vitamin B1)
- nutrient_topic
- Thiamine research collection; topical membership is not evidence of a direct dietary effect. · Thiamine (vitamin B1)
- organism
- Cricetulus griseus
- plain_language
- In these hamster cells, the ER lyase made the larger contribution to disposal of this sphingoid-base-derived substrate.
- primary_references
- [kitamura-2017-hacl2] Phytosphingosine degradation pathway includes fatty acid α-oxidation reactions in the endoplasmic reticulum (2017). https://pubmed.ncbi.nlm.nih.gov/28289220/ DOI: 10.1073/pnas.1700138114
- tissue_or_cell_type
- Ovary-derived CHO-K1 cells
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Thiamine: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1044–1055
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · CHO-K1 knockout and radiolabeled phytosphingosine tracing. · source_derived_draft · unverified_draft
### b1-hamster-hacl2-phytosphingosine-flux Hacl2 knockout reduced phytosphingosine-derived glycerolipid labeling more strongly than Hacl1 knockout in CHO-K1 cells. Condition category: machinery_impairment nutrient_topic: Thiamine research collection; topical membership is not evidence of a direct dietary effect. plain_language: In these hamster cells, the ER lyase made the larger contribution to disposal of this sphingoid-base-derived substrate. organism: Cricetulus griseus tissue_or_cell_type: Ovary-derived CHO-K1 cells experimental_model: CHO-K1 knockout and radiolabeled phytosphingosine tracing. limitations: Genetic cell model; does not establish human tissue dominance or thiamine-deficiency pathology. evidence: [{"paper_key": "kitamura-2017-hacl2", "source_bundle": "artifacts/thiamine_metabolism_sources.json", "passage_ids": ["p-42", "p-61"], "locator": "higher contribution of HACL2", "preservation": "Exact text retained in the source bundle; full source document retained when openly retrievable."}] nutrient: Thiamine (vitamin B1) [kitamura-2017-hacl2] Phytosphingosine degradation pathway includes fatty acid α-oxidation reactions in the endoplasmic reticulum (2017). https://pubmed.ncbi.nlm.nih.gov/28289220/ DOI: 10.1073/pnas.1700138114
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.