Component

Human histone deacetylase 6 / HDAC6

Human histone deacetylase 6 / HDAC6. Species, exposure and limitations are retained in each linked claim.

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 acts on it

  1. HDAC6 protein decreased early during treatment and HDAC6 transcript was suppressed after 48 hours.

    Sulforaphane / SFN, stereochemistry specified per study → Human histone deacetylase 6 / HDAC6 source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/sulforaphane-research/25307283.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "cc736d6c2f2dc6c4026bdad0a5835d69ed094775076a2c1606f47020e6783331", "start_char": 0, "end_char": 1504, "text_sha256": "cc736d6c2f2dc6c4026bdad0a5835d69ed094775076a2c1606f47020e6783331"}
    experimental_model
    Matched cell-type and time-course comparison
    exposure
    Sulforaphane exposure; serum and time-course comparisons
    limitations
    Activity assays, protein abundance and substrate acetylation are distinct endpoints; mechanism of their divergence was not established. Erratum PMID 27271518 adds an omitted funding acknowledgment without revising these results.
    nutrient_topic
    Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. · Sulforaphane / SFN, stereochemistry specified per study
    organism
    Human HaCaT keratinocytes and HCT116 colon cancer cells
    plain_language
    Protein abundance and catalytic activity must be recorded separately.
    primary_references
    [sulforaphane-p25307283] The effect of sulforaphane on histone deacetylase activity in keratinocytes: Differences between in vitro and in vivo analyses. (2015). https://pubmed.ncbi.nlm.nih.gov/25307283/ DOI: 10.1002/mc.22224
    tissue_or_cell_type
    HDAC activity, protein levels and target acetylation

    Sulforaphane: formation, electrophile sensing and nutrient connections (2026-09-17) · lines 619–630

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Matched cell-type and time-course comparison · source_derived_draft · unverified_draft

    ### sulforaphane-hdac6-abundance HDAC6 protein decreased early during treatment and HDAC6 transcript was suppressed after 48 hours. Condition category: normal nutrient_topic: Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. plain_language: Protein abundance and catalytic activity must be recorded separately. organism: Human HaCaT keratinocytes and HCT116 colon cancer cells tissue_or_cell_type: HDAC activity, protein levels and target acetylation experimental_model: Matched cell-type and time-course comparison limitations: Activity assays, protein abundance and substrate acetylation are distinct endpoints; mechanism of their divergence was not established. Erratum PMID 27271518 adds an omitted funding acknowledgment without revising these results. exposure: Sulforaphane exposure; serum and time-course comparisons evidence_span: {"source_cache": "artifacts/sulforaphane-research/25307283.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "cc736d6c2f2dc6c4026bdad0a5835d69ed094775076a2c1606f47020e6783331", "start_char": 0, "end_char": 1504, "text_sha256": "cc736d6c2f2dc6c4026bdad0a5835d69ed094775076a2c1606f47020e6783331"} [sulforaphane-p25307283] The effect of sulforaphane on histone deacetylase activity in keratinocytes: Differences between in vitro and in vivo analyses. (2015). https://pubmed.ncbi.nlm.nih.gov/25307283/ DOI: 10.1002/mc.22224
    Complete structured claim and evidence

  2. Sulforaphane inhibited cytoplasmic HDAC6 activity in the U2OS study.

    Sulforaphane / SFN, stereochemistry specified per study → Human histone deacetylase 6 / HDAC6 source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/sulforaphane-research/31409554.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5486f97c1271a771620cdf2e6245a54ff63f3f56b3eb884f201fda9882ec947b", "start_char": 0, "end_char": 1778, "text_sha256": "5486f97c1271a771620cdf2e6245a54ff63f3f56b3eb884f201fda9882ec947b"}
    experimental_model
    Human cell experiments with CRISPR NRF2 deletion
    exposure
    Concentration- and time-dependent sulforaphane treatment
    limitations
    Preclinical cancer-cell signaling; AKT phosphorylation did not reliably represent catalytic output. Not a human longevity or autophagy trial.
    nutrient_topic
    Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. · Sulforaphane / SFN, stereochemistry specified per study
    organism
    Human U2OS osteosarcoma cells and NRF2-knockout counterpart
    plain_language
    This experiment identifies a particular HDAC isoform.
    primary_references
    [sulforaphane-p31409554] The isothiocyanate sulforaphane inhibits mTOR in an NRF2-independent manner. (2021). https://pubmed.ncbi.nlm.nih.gov/31409554/ DOI: 10.1016/j.phymed.2019.153062
    tissue_or_cell_type
    HDAC6, AKT and mTOR signaling

    Sulforaphane: formation, electrophile sensing and nutrient connections (2026-09-17) · lines 645–656

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human cell experiments with CRISPR NRF2 deletion · source_derived_draft · unverified_draft

    ### sulforaphane-hdac6-activity Sulforaphane inhibited cytoplasmic HDAC6 activity in the U2OS study. Condition category: normal nutrient_topic: Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. plain_language: This experiment identifies a particular HDAC isoform. organism: Human U2OS osteosarcoma cells and NRF2-knockout counterpart tissue_or_cell_type: HDAC6, AKT and mTOR signaling experimental_model: Human cell experiments with CRISPR NRF2 deletion limitations: Preclinical cancer-cell signaling; AKT phosphorylation did not reliably represent catalytic output. Not a human longevity or autophagy trial. exposure: Concentration- and time-dependent sulforaphane treatment evidence_span: {"source_cache": "artifacts/sulforaphane-research/31409554.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5486f97c1271a771620cdf2e6245a54ff63f3f56b3eb884f201fda9882ec947b", "start_char": 0, "end_char": 1778, "text_sha256": "5486f97c1271a771620cdf2e6245a54ff63f3f56b3eb884f201fda9882ec947b"} [sulforaphane-p31409554] The isothiocyanate sulforaphane inhibits mTOR in an NRF2-independent manner. (2021). https://pubmed.ncbi.nlm.nih.gov/31409554/ DOI: 10.1016/j.phymed.2019.153062
    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