Component

2-Hydroxystearate

Free 2-hydroxy-C18:0 fatty acid, distinct from its CoA ester.

2 recorded relationships. Experimental role, claim status and evidence remain attached to each record.

Read recorded mechanisms Open recursive mind map

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.

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.

Recorded relationships

What it acts on

  1. Rat liver/hepatocyte pathway experiments supported activation of 2-hydroxy-fatty acid to its CoA ester before ThDP-dependent cleavage; whole-pathway assays required ATP, CoA, Mg2+, ThDP and NAD+.

    2-Hydroxystearate → 2-Hydroxystearoyl-CoA source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    B1 cleavage is sequentially coupled to B5-derived CoA activation and B3-related NAD oxidation.
    evidence
    [{"paper_key": "foulon-2005-hacl1", "source_bundle": "artifacts/thiamine_metabolism_sources.json", "passage_ids": ["abstract"], "locator": "Primary publication abstract", "preservation": "Exact text retained in the source bundle; full source document retained when openly retrievable."}]
    experimental_model
    Intact/permeabilized rat hepatocytes and liver preparations.
    limitations
    Whole-pathway requirements cannot all be assigned to the isolated lyase.
    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
    Rattus norvegicus
    plain_language
    ATP activates the fatty acid upstream, while NAD supports later oxidation. Listing all pathway cofactors does not mean HACL itself consumes ATP or NAD.
    primary_references
    [foulon-2005-hacl1] Breakdown of 2-hydroxylated straight chain fatty acids via peroxisomal 2-hydroxyphytanoyl-CoA lyase: a revised pathway for the alpha-oxidation of straight chain fatty acids (2005). https://pubmed.ncbi.nlm.nih.gov/15644336/ DOI: 10.1074/jbc.m413362200
    tissue_or_cell_type
    Liver

    Thiamine: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1003–1015

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Intact/permeabilized rat hepatocytes and liver preparations. · source_derived_draft · unverified_draft

    ### b1-alpha-oxidation-activation-before-cleavage Rat liver/hepatocyte pathway experiments supported activation of 2-hydroxy-fatty acid to its CoA ester before ThDP-dependent cleavage; whole-pathway assays required ATP, CoA, Mg2+, ThDP and NAD+. Condition category: normal nutrient_topic: Thiamine research collection; topical membership is not evidence of a direct dietary effect. plain_language: ATP activates the fatty acid upstream, while NAD supports later oxidation. Listing all pathway cofactors does not mean HACL itself consumes ATP or NAD. organism: Rattus norvegicus tissue_or_cell_type: Liver experimental_model: Intact/permeabilized rat hepatocytes and liver preparations. limitations: Whole-pathway requirements cannot all be assigned to the isolated lyase. evidence: [{"paper_key": "foulon-2005-hacl1", "source_bundle": "artifacts/thiamine_metabolism_sources.json", "passage_ids": ["abstract"], "locator": "Primary publication abstract", "preservation": "Exact text retained in the source bundle; full source document retained when openly retrievable."}] cross_nutrient: B1 cleavage is sequentially coupled to B5-derived CoA activation and B3-related NAD oxidation. nutrient: Thiamine (vitamin B1) [foulon-2005-hacl1] Breakdown of 2-hydroxylated straight chain fatty acids via peroxisomal 2-hydroxyphytanoyl-CoA lyase: a revised pathway for the alpha-oxidation of straight chain fatty acids (2005). https://pubmed.ncbi.nlm.nih.gov/15644336/ DOI: 10.1074/jbc.m413362200
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Affinity-purified human HACL2 produced fatty aldehyde from 2-hydroxy-C18:0-CoA, but not the free acid, and activity depended on added ThDP.

    Human 2-hydroxyacyl-CoA lyase 2 / HACL2 → 2-Hydroxystearoyl-CoA source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    B1-dependent cleavage uses a B5-derived CoA-ester substrate.
    evidence
    [{"paper_key": "kitamura-2017-hacl2", "source_bundle": "artifacts/thiamine_metabolism_sources.json", "passage_ids": ["p-32"], "locator": "generated fatty aldehyde", "preservation": "Exact text retained in the source bundle; full source document retained when openly retrievable."}]
    experimental_model
    Human tagged HACL2 purified from HEK293T cells.
    limitations
    Aldehyde detected by TLC/Schiff staining; expected C17 identity is not a separate mass-spectrometric assignment. Mg omission was not this experiment.
    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
    Homo sapiens
    plain_language
    B1 supports HACL2 cleavage only after the fatty acid has been activated onto CoA.
    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
    Purified membrane-associated protein

    Thiamine: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1017–1029

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human tagged HACL2 purified from HEK293T cells. · source_derived_draft · unverified_draft

    ### b1-hacl2-thdp-dependent-coa-cleavage Affinity-purified human HACL2 produced fatty aldehyde from 2-hydroxy-C18:0-CoA, but not the free acid, and activity depended on added ThDP. Condition category: normal nutrient_topic: Thiamine research collection; topical membership is not evidence of a direct dietary effect. plain_language: B1 supports HACL2 cleavage only after the fatty acid has been activated onto CoA. organism: Homo sapiens tissue_or_cell_type: Purified membrane-associated protein experimental_model: Human tagged HACL2 purified from HEK293T cells. limitations: Aldehyde detected by TLC/Schiff staining; expected C17 identity is not a separate mass-spectrometric assignment. Mg omission was not this experiment. evidence: [{"paper_key": "kitamura-2017-hacl2", "source_bundle": "artifacts/thiamine_metabolism_sources.json", "passage_ids": ["p-32"], "locator": "generated fatty aldehyde", "preservation": "Exact text retained in the source bundle; full source document retained when openly retrievable."}] cross_nutrient: B1-dependent cleavage uses a B5-derived CoA-ester substrate. 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

In the sources

Preserved passages that mention this component, quoted exactly. Open one to read it in context.

    This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.

    Evidence, AI assistance and curation standards