Component

Mouse forkhead transcription factor Foxo1

Mouse forkhead transcription factor Foxo1. Species, exposure and limitations are retained in each linked claim.

3 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. Foxo1 acted as a direct repressor of IL-23 receptor expression in the study.

    Mouse forkhead transcription factor Foxo1 → Mouse IL-23 receptor expression source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/sodium-research/23467085.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "25fdc34faa9d6f0b84dfc9daf98ecc8e09f2486853b9e99bdae552e5ca8c5b2e", "start_char": 0, "end_char": 1656, "text_sha256": "25fdc34faa9d6f0b84dfc9daf98ecc8e09f2486853b9e99bdae552e5ca8c5b2e"}
    experimental_model
    T-cell transcriptional profiling, kinase loss and experimental autoimmune assays
    exposure
    NaCl elevation and Sgk1 perturbation
    limitations
    The SGK1–Foxo1–IL23R pathway is scoped to this immune-cell program, not universal sodium action.
    nutrient_topic
    Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
    organism
    Mouse
    plain_language
    Turning down a repressor can let a receptor become more abundant.
    primary_references
    [sodium-p23467085] Induction of pathogenic TH17 cells by inducible salt-sensing kinase SGK1. (2013). https://pubmed.ncbi.nlm.nih.gov/23467085/ DOI: 10.1038/nature11984
    tissue_or_cell_type
    IL-23-responsive TH17 cells

    Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 564–575

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · T-cell transcriptional profiling, kinase loss and experimental autoimmune assays · source_derived_draft · unverified_draft

    ### sodium-foxo-il23r Foxo1 acted as a direct repressor of IL-23 receptor expression in the study. Condition category: normal nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Turning down a repressor can let a receptor become more abundant. organism: Mouse tissue_or_cell_type: IL-23-responsive TH17 cells experimental_model: T-cell transcriptional profiling, kinase loss and experimental autoimmune assays limitations: The SGK1–Foxo1–IL23R pathway is scoped to this immune-cell program, not universal sodium action. exposure: NaCl elevation and Sgk1 perturbation evidence_span: {"source_cache": "artifacts/sodium-research/23467085.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "25fdc34faa9d6f0b84dfc9daf98ecc8e09f2486853b9e99bdae552e5ca8c5b2e", "start_char": 0, "end_char": 1656, "text_sha256": "25fdc34faa9d6f0b84dfc9daf98ecc8e09f2486853b9e99bdae552e5ca8c5b2e"} [sodium-p23467085] Induction of pathogenic TH17 cells by inducible salt-sensing kinase SGK1. (2013). https://pubmed.ncbi.nlm.nih.gov/23467085/ DOI: 10.1038/nature11984
    Complete structured claim and evidence

What acts on it

  1. The study identified SGK1-dependent deactivation of Foxo1 in the TH17 program.

    Serum and glucocorticoid-regulated kinase 1 → Mouse forkhead transcription factor Foxo1 source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/sodium-research/23467085.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "25fdc34faa9d6f0b84dfc9daf98ecc8e09f2486853b9e99bdae552e5ca8c5b2e", "start_char": 0, "end_char": 1656, "text_sha256": "25fdc34faa9d6f0b84dfc9daf98ecc8e09f2486853b9e99bdae552e5ca8c5b2e"}
    experimental_model
    T-cell transcriptional profiling, kinase loss and experimental autoimmune assays
    exposure
    NaCl elevation and Sgk1 perturbation
    limitations
    The SGK1–Foxo1–IL23R pathway is scoped to this immune-cell program, not universal sodium action.
    nutrient_topic
    Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
    organism
    Mouse
    plain_language
    The same kinase family used in kidney salt handling has another role in immune cells.
    primary_references
    [sodium-p23467085] Induction of pathogenic TH17 cells by inducible salt-sensing kinase SGK1. (2013). https://pubmed.ncbi.nlm.nih.gov/23467085/ DOI: 10.1038/nature11984
    tissue_or_cell_type
    IL-23-responsive TH17 cells

    Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 551–562

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · T-cell transcriptional profiling, kinase loss and experimental autoimmune assays · source_derived_draft · unverified_draft

    ### sodium-sgk-foxo The study identified SGK1-dependent deactivation of Foxo1 in the TH17 program. Condition category: normal nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The same kinase family used in kidney salt handling has another role in immune cells. organism: Mouse tissue_or_cell_type: IL-23-responsive TH17 cells experimental_model: T-cell transcriptional profiling, kinase loss and experimental autoimmune assays limitations: The SGK1–Foxo1–IL23R pathway is scoped to this immune-cell program, not universal sodium action. exposure: NaCl elevation and Sgk1 perturbation evidence_span: {"source_cache": "artifacts/sodium-research/23467085.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "25fdc34faa9d6f0b84dfc9daf98ecc8e09f2486853b9e99bdae552e5ca8c5b2e", "start_char": 0, "end_char": 1656, "text_sha256": "25fdc34faa9d6f0b84dfc9daf98ecc8e09f2486853b9e99bdae552e5ca8c5b2e"} [sodium-p23467085] Induction of pathogenic TH17 cells by inducible salt-sensing kinase SGK1. (2013). https://pubmed.ncbi.nlm.nih.gov/23467085/ DOI: 10.1038/nature11984
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Foxo3 deletion, unlike Foxo1 deletion, made mouse stem/progenitor cells resistant to butyrate-mediated proliferation suppression.

    Mouse forkhead transcription factor Foxo3 → Mouse colonic stem/progenitor-cell proliferation source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary full text, Figure 7
    experimental_model
    Mouse genetic stem-cell experiments.
    limitations
    Loss of a response is not rescue of a nutrient deficiency. Correction record: A published erratum is confirmed by PubMed and publisher/Crossref metadata: Cell 167(4):1137, 2016. The notice body was not available through the accessed publisher endpoints. The main article's Acads/Foxo3 and crypt experiments were read, but the specific effect of the correction remains unassessed. https://pubmed.ncbi.nlm.nih.gov/27814510/
    nutrient_topic
    Butyrate collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Butyrate
    plain_language
    The growth-suppressing response depended on a specific transcription factor.
    primary_references
    The Colonic Crypt Protects Stem Cells from Microbiota-Derived Metabolites. · 2016 · https://pubmed.ncbi.nlm.nih.gov/27264604/ · DOI 10.1016/j.cell.2016.05.018
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Butyrate: microbial production, fuel use, signaling and nutrient interactions (2026-09-19) · lines 326–332

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mouse genetic stem-cell experiments. · source_derived_draft · unverified_draft

    ## butyrate-foxo3-loss The growth-suppressing response depended on a specific transcription factor. Foxo3 deletion, unlike Foxo1 deletion, made mouse stem/progenitor cells resistant to butyrate-mediated proliferation suppression. Model: Mouse genetic stem-cell experiments. Limitations: Loss of a response is not rescue of a nutrient deficiency. Correction record: A published erratum is confirmed by PubMed and publisher/Crossref metadata: Cell 167(4):1137, 2016. The notice body was not available through the accessed publisher endpoints. The main article's Acads/Foxo3 and crypt experiments were read, but the specific effect of the correction remains unassessed. https://pubmed.ncbi.nlm.nih.gov/27814510/ Evidence access: Primary full text, Figure 7 The Colonic Crypt Protects Stem Cells from Microbiota-Derived Metabolites. · 2016 · https://pubmed.ncbi.nlm.nih.gov/27264604/ · DOI 10.1016/j.cell.2016.05.018
    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