Component

Human hepatocyte nuclear factor 1 alpha / HNF1A

Human hepatocyte nuclear factor 1 alpha / HNF1A. Species, exposure and limitations are retained in each linked claim.

5 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. Berberine accelerated ubiquitin-associated proteasomal degradation of HNF1A protein in HepG2 cells.

    Berberine → Human hepatocyte nuclear factor 1 alpha / HNF1A source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/berberine-research/25540198.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "08c835c28631cd0c79be4e5a602216f8eddcd0f2d0c967074d7c9faf4aa9e446", "start_char": 0, "end_char": 1769, "text_sha256": "08c835c28631cd0c79be4e5a602216f8eddcd0f2d0c967074d7c9faf4aa9e446"}
    experimental_model
    Protein-turnover and proteasome-inhibitor experiments
    exposure
    Berberine, ubiquitin assays and proteasome inhibition
    limitations
    HNF1A protein turnover differs from HNF1A gene transcription. Proteasome inhibitors are experimental probes, not suggested combination treatment.
    nutrient_topic
    Berberine research collection; topical membership is not evidence of a direct dietary effect. · Berberine
    organism
    Human HepG2 cells; separate mouse and hamster arms
    plain_language
    The cell made less of a cholesterol-regulating signal because its upstream regulator was degraded.
    primary_references
    [berberine-p25540198] Inhibition of PCSK9 transcription by berberine involves down-regulation of hepatic HNF1α protein expression through the ubiquitin-proteasome degradation pathway. (2015). https://pubmed.ncbi.nlm.nih.gov/25540198/ DOI: 10.1074/jbc.m114.597229
    tissue_or_cell_type
    HNF1A and PCSK9 gene regulation

    Berberine: metabolism, nutrient connections and drug interactions (2026-09-17) · lines 467–478

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Protein-turnover and proteasome-inhibitor experiments · source_derived_draft · unverified_draft

    ### berberine-hnf1a-degradation Berberine accelerated ubiquitin-associated proteasomal degradation of HNF1A protein in HepG2 cells. Condition category: normal nutrient_topic: Berberine research collection; topical membership is not evidence of a direct dietary effect. plain_language: The cell made less of a cholesterol-regulating signal because its upstream regulator was degraded. organism: Human HepG2 cells; separate mouse and hamster arms tissue_or_cell_type: HNF1A and PCSK9 gene regulation experimental_model: Protein-turnover and proteasome-inhibitor experiments limitations: HNF1A protein turnover differs from HNF1A gene transcription. Proteasome inhibitors are experimental probes, not suggested combination treatment. exposure: Berberine, ubiquitin assays and proteasome inhibition evidence_span: {"source_cache": "artifacts/berberine-research/25540198.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "08c835c28631cd0c79be4e5a602216f8eddcd0f2d0c967074d7c9faf4aa9e446", "start_char": 0, "end_char": 1769, "text_sha256": "08c835c28631cd0c79be4e5a602216f8eddcd0f2d0c967074d7c9faf4aa9e446"} [berberine-p25540198] Inhibition of PCSK9 transcription by berberine involves down-regulation of hepatic HNF1α protein expression through the ubiquitin-proteasome degradation pathway. (2015). https://pubmed.ncbi.nlm.nih.gov/25540198/ DOI: 10.1074/jbc.m114.597229
    Complete structured claim and evidence

  2. Combining RNA sequencing analysis, the decrease in hepatitis B virus transcriptional activity by (-)-lariciresinol was reported as possibly related to hepatocyte nuclear factor 1 alpha, and the compound was described as inhibiting replication by regulating HNF1α-mediated transcription.

    (-)-Lariciresinol → Human hepatocyte nuclear factor 1 alpha / HNF1A source_derived_draftungraded
    Experimental context and source evidence
    duration
    Not stated here
    evidence_access
    Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    experimental_model
    Hepatoma cells carrying hepatitis B virus, with RNA sequencing
    exposure
    (-)-Lariciresinol isolated from the roots of Isatis indigotica
    limitations
    The abstract hedges the link as one that may be related, and states regulation without giving a direction, a magnitude or a concentration, so no direction is recorded. No knockdown or over-expression rescue of HNF1α is described in the abstract, so the relationship is associative rather than demonstrated as necessary.
    organism
    Hepatoma cells carrying hepatitis B virus, with RNA sequencing
    plain_language
    Combining RNA sequencing analysis, the decrease in hepatitis B virus transcriptional activity by (-)-lariciresinol was reported as possibly related to hepatocyte nuclear factor 1 alpha, and the compound was described as inhibiting replication by regulating HNF1α-mediated transcription.
    primary_references
    (-)-Lariciresinol Isolated from the Roots of Isatis indigotica Fortune ex Lindl. Inhibits Hepatitis B Virus by Regulating Viral Transcription. (2022). https://pubmed.ncbi.nlm.nih.gov/35630700/ DOI: 10.3390/molecules27103223
    route
    In vitro
    tissue
    Host transcription factor and viral transcriptional activity

    (-)-Lariciresinol and hepatocyte nuclear factor 1 alpha: the host-factor step (2026-09-22) · lines 11–20

    Original AI-assisted curation of twelve primary studies, every abstract read and all DOIs cross-checked against live PubMed metadata. Mechanism edges only, with no conclusion or claim of benefit recorded. Three author clusters account for eight of the twelve and carry shared laboratory keys. Study-specific concentrations, negative findings and limitations retained. Not publisher full text. · supports · · source_derived_draft · unverified_draft

    ## minus-lariciresinol-regulates-hnf1-alpha Combining RNA sequencing analysis, the decrease in hepatitis B virus transcriptional activity by (-)-lariciresinol was reported as possibly related to hepatocyte nuclear factor 1 alpha, and the compound was described as inhibiting replication by regulating HNF1α-mediated transcription. Model/species: Hepatoma cells carrying hepatitis B virus, with RNA sequencing Tissue/system: Host transcription factor and viral transcriptional activity Exposure: (-)-Lariciresinol isolated from the roots of Isatis indigotica Route: In vitro Duration: Not stated here Limits: The abstract hedges the link as one that may be related, and states regulation without giving a direction, a magnitude or a concentration, so no direction is recorded. No knockdown or over-expression rescue of HNF1α is described in the abstract, so the relationship is associative rather than demonstrated as necessary. Primary reference: (-)-Lariciresinol Isolated from the Roots of Isatis indigotica Fortune ex Lindl. Inhibits Hepatitis B Virus by Regulating Viral Transcription. (2022). https://pubmed.ncbi.nlm.nih.gov/35630700/ DOI: 10.3390/molecules27103223 Access: Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Berberine lowered HNF1A-dependent PCSK9 transcription; proteasome inhibition prevented this response.

    Berberine → PCSK9 transcription source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/berberine-research/25540198.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "08c835c28631cd0c79be4e5a602216f8eddcd0f2d0c967074d7c9faf4aa9e446", "start_char": 0, "end_char": 1769, "text_sha256": "08c835c28631cd0c79be4e5a602216f8eddcd0f2d0c967074d7c9faf4aa9e446"}
    experimental_model
    Protein-turnover and proteasome-inhibitor experiments
    exposure
    Berberine, ubiquitin assays and proteasome inhibition
    limitations
    HNF1A protein turnover differs from HNF1A gene transcription. Proteasome inhibitors are experimental probes, not suggested combination treatment.
    nutrient_topic
    Berberine research collection; topical membership is not evidence of a direct dietary effect. · Berberine
    organism
    Human HepG2 cells; separate mouse and hamster arms
    plain_language
    This route regulates a protein that controls LDL-receptor availability.
    primary_references
    [berberine-p25540198] Inhibition of PCSK9 transcription by berberine involves down-regulation of hepatic HNF1α protein expression through the ubiquitin-proteasome degradation pathway. (2015). https://pubmed.ncbi.nlm.nih.gov/25540198/ DOI: 10.1074/jbc.m114.597229
    tissue_or_cell_type
    HNF1A and PCSK9 gene regulation

    Berberine: metabolism, nutrient connections and drug interactions (2026-09-17) · lines 480–491

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Protein-turnover and proteasome-inhibitor experiments · source_derived_draft · unverified_draft

    ### berberine-pcsk9-transcription Berberine lowered HNF1A-dependent PCSK9 transcription; proteasome inhibition prevented this response. Condition category: normal nutrient_topic: Berberine research collection; topical membership is not evidence of a direct dietary effect. plain_language: This route regulates a protein that controls LDL-receptor availability. organism: Human HepG2 cells; separate mouse and hamster arms tissue_or_cell_type: HNF1A and PCSK9 gene regulation experimental_model: Protein-turnover and proteasome-inhibitor experiments limitations: HNF1A protein turnover differs from HNF1A gene transcription. Proteasome inhibitors are experimental probes, not suggested combination treatment. exposure: Berberine, ubiquitin assays and proteasome inhibition evidence_span: {"source_cache": "artifacts/berberine-research/25540198.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "08c835c28631cd0c79be4e5a602216f8eddcd0f2d0c967074d7c9faf4aa9e446", "start_char": 0, "end_char": 1769, "text_sha256": "08c835c28631cd0c79be4e5a602216f8eddcd0f2d0c967074d7c9faf4aa9e446"} [berberine-p25540198] Inhibition of PCSK9 transcription by berberine involves down-regulation of hepatic HNF1α protein expression through the ubiquitin-proteasome degradation pathway. (2015). https://pubmed.ncbi.nlm.nih.gov/25540198/ DOI: 10.1074/jbc.m114.597229
    Complete structured claim and evidence

  2. (-)-Lariciresinol dose-dependently inhibited other animal hepadnaviruses, including woodchuck hepatitis virus and duck hepatitis B virus.

    (-)-Lariciresinol → Woodchuck hepatitis virus and duck hepatitis B virus replication source_derived_draftungraded
    Experimental context and source evidence
    duration
    Not stated here
    evidence_access
    Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    experimental_model
    Cell systems carrying woodchuck hepatitis virus and duck hepatitis B virus
    exposure
    (-)-Lariciresinol, dose-dependent
    limitations
    Activity across three hepadnaviruses is consistent with a host target rather than a viral enzyme, but the abstract does not give the concentrations or the size of the reduction for each virus.
    organism
    Cell systems carrying woodchuck hepatitis virus and duck hepatitis B virus
    plain_language
    (-)-Lariciresinol dose-dependently inhibited other animal hepadnaviruses, including woodchuck hepatitis virus and duck hepatitis B virus.
    primary_references
    (-)-Lariciresinol Isolated from the Roots of Isatis indigotica Fortune ex Lindl. Inhibits Hepatitis B Virus by Regulating Viral Transcription. (2022). https://pubmed.ncbi.nlm.nih.gov/35630700/ DOI: 10.3390/molecules27103223
    route
    In vitro
    tissue
    Hepadnaviral replication across species

    (-)-Lariciresinol and hepatocyte nuclear factor 1 alpha: the host-factor step (2026-09-22) · lines 22–31

    Original AI-assisted curation of twelve primary studies, every abstract read and all DOIs cross-checked against live PubMed metadata. Mechanism edges only, with no conclusion or claim of benefit recorded. Three author clusters account for eight of the twelve and carry shared laboratory keys. Study-specific concentrations, negative findings and limitations retained. Not publisher full text. · supports · · source_derived_draft · unverified_draft

    ## minus-lariciresinol-inhibits-other-hepadnaviruses (-)-Lariciresinol dose-dependently inhibited other animal hepadnaviruses, including woodchuck hepatitis virus and duck hepatitis B virus. Model/species: Cell systems carrying woodchuck hepatitis virus and duck hepatitis B virus Tissue/system: Hepadnaviral replication across species Exposure: (-)-Lariciresinol, dose-dependent Route: In vitro Duration: Not stated here Limits: Activity across three hepadnaviruses is consistent with a host target rather than a viral enzyme, but the abstract does not give the concentrations or the size of the reduction for each virus. Primary reference: (-)-Lariciresinol Isolated from the Roots of Isatis indigotica Fortune ex Lindl. Inhibits Hepatitis B Virus by Regulating Viral Transcription. (2022). https://pubmed.ncbi.nlm.nih.gov/35630700/ DOI: 10.3390/molecules27103223 Access: Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    Complete structured claim and evidence

  3. (−)-Lariciresinol blocked hepatitis B virus RNA production first, followed by viral proteins, then viral particles and DNA.

    (-)-Lariciresinol → Hepatitis B virus RNA production source_derived_draftungraded
    Experimental context and source evidence
    duration
    Time course, order established by sequence of loss
    evidence_access
    Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    experimental_model
    Hepatoma cell lines carrying hepatitis B virus
    exposure
    (−)-Lariciresinol isolated from the roots of Isatis indigotica
    limitations
    The order of events is what the time course establishes; the abstract does not give the concentrations at which each step was measured.
    organism
    Hepatoma cell lines carrying hepatitis B virus
    plain_language
    (−)-Lariciresinol blocked hepatitis B virus RNA production first, followed by viral proteins, then viral particles and DNA.
    primary_references
    Anti-Hepatitis B Virus Activity of (-)-Lariciresinol Isolated from the Roots of Isatis indigotica. (2022). https://pubmed.ncbi.nlm.nih.gov/35630700/ DOI: 10.3390/molecules27103180
    route
    In vitro
    tissue
    Viral RNA, protein and particle production in order of appearance

    Lariciresinol: five molecules under one name, and the mechanisms each one carries (2026-09-22) · lines 77–86

    Original AI-assisted curation of twelve primary studies, every abstract read and all DOIs cross-checked against live PubMed metadata. Mechanism edges only, with no conclusion or claim of benefit recorded. Three author clusters account for eight of the twelve and carry shared laboratory keys. Study-specific concentrations, negative findings and limitations retained. Not publisher full text. · supports · · source_derived_draft · unverified_draft

    ## minus-lariciresinol-lowers-hepatitis-b-rna (−)-Lariciresinol blocked hepatitis B virus RNA production first, followed by viral proteins, then viral particles and DNA. Model/species: Hepatoma cell lines carrying hepatitis B virus Tissue/system: Viral RNA, protein and particle production in order of appearance Exposure: (−)-Lariciresinol isolated from the roots of Isatis indigotica Route: In vitro Duration: Time course, order established by sequence of loss Limits: The order of events is what the time course establishes; the abstract does not give the concentrations at which each step was measured. Primary reference: Anti-Hepatitis B Virus Activity of (-)-Lariciresinol Isolated from the Roots of Isatis indigotica. (2022). https://pubmed.ncbi.nlm.nih.gov/35630700/ DOI: 10.3390/molecules27103180 Access: Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    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