Component

Intracellular myo-inositol availability

Intracellular myo-inositol availability. Species, exposure and limitations are retained in each linked claim.

3 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.

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. HMIT-null mice did not show altered inositol transport or homeostasis in the reported analyses.

    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/inositol-research/19607714.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "8b8bd010f44dd8b055efc345c57791e88547114b0a2f27d782183674fc53f984", "start_char": 0, "end_char": 1332, "text_sha256": "8b8bd010f44dd8b055efc345c57791e88547114b0a2f27d782183674fc53f984"}
    experimental_model
    Immunolocalization, neuronal electrophysiology and knockout
    exposure
    Native localization and HMIT-null comparisons
    limitations
    Native localization qualifies earlier heterologous uptake findings; it is an explained context difference, not evidence that one experiment is false.
    nutrient_topic
    Inositol research collection; topical membership is not evidence of a direct dietary effect. · Inositol (stereoisomer family)
    organism
    Rat and human brain; mouse knockout
    plain_language
    Removing this one candidate transporter did not produce the predicted general uptake failure.
    primary_references
    [ino-p19607714] Evaluation of expression and function of the H+/myo-inositol transporter HMIT. (2009). https://pubmed.ncbi.nlm.nih.gov/19607714/ DOI: 10.1186/1471-2121-10-54
    tissue_or_cell_type
    Brain neurons and cultured neurons
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Inositol: synthesis, signaling, mineral interactions and conditional deficiency (2026-09-17) · lines 392–403

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Immunolocalization, neuronal electrophysiology and knockout · source_derived_draft · unverified_draft

    ### ino-hmit-null HMIT-null mice did not show altered inositol transport or homeostasis in the reported analyses. Condition category: machinery_impairment nutrient_topic: Inositol research collection; topical membership is not evidence of a direct dietary effect. plain_language: Removing this one candidate transporter did not produce the predicted general uptake failure. organism: Rat and human brain; mouse knockout tissue_or_cell_type: Brain neurons and cultured neurons experimental_model: Immunolocalization, neuronal electrophysiology and knockout limitations: Native localization qualifies earlier heterologous uptake findings; it is an explained context difference, not evidence that one experiment is false. exposure: Native localization and HMIT-null comparisons evidence_span: {"source_cache": "artifacts/inositol-research/19607714.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "8b8bd010f44dd8b055efc345c57791e88547114b0a2f27d782183674fc53f984", "start_char": 0, "end_char": 1332, "text_sha256": "8b8bd010f44dd8b055efc345c57791e88547114b0a2f27d782183674fc53f984"} [ino-p19607714] Evaluation of expression and function of the H+/myo-inositol transporter HMIT. (2009). https://pubmed.ncbi.nlm.nih.gov/19607714/ DOI: 10.1186/1471-2121-10-54
    Complete structured claim and evidence
  2. At 0.6 mM valproate, yeast expressing human ISYNA1 had approximately 25% less intracellular inositol; purified ISYNA1 was not inhibited at that concentration.

    Valproate → Intracellular myo-inositol availability source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/inositol-research/15024000.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5ab3a8eda77989c3e4a681b4a971fb7e969c285d3e5c8e41bc31713a7f88c9ac", "start_char": 0, "end_char": 1427, "text_sha256": "5ab3a8eda77989c3e4a681b4a971fb7e969c285d3e5c8e41bc31713a7f88c9ac"}
    experimental_model
    Recombinant human enzyme and complementation of yeast ino1 deletion
    exposure
    Substrate, NAD+, cation and valproate experiments
    limitations
    Purified-enzyme and yeast results do not establish supplement effects or a human dietary deficiency threshold.
    nutrient_topic
    Inositol research collection; topical membership is not evidence of a direct dietary effect. · Inositol (stereoisomer family)
    organism
    Human protein expressed in bacteria and yeast
    plain_language
    The effect depended on the cellular setting rather than direct inhibition of the isolated enzyme.
    primary_references
    [ino-p15024000] Human 1-D-myo-inositol-3-phosphate synthase is functional in yeast. (2004). https://pubmed.ncbi.nlm.nih.gov/15024000/ DOI: 10.1074/jbc.m312078200
    tissue_or_cell_type
    Purified enzyme; yeast cultures
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Inositol: synthesis, signaling, mineral interactions and conditional deficiency (2026-09-17) · lines 223–234

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Recombinant human enzyme and complementation of yeast ino1 deletion · source_derived_draft · unverified_draft

    ### ino-valproate-yeast At 0.6 mM valproate, yeast expressing human ISYNA1 had approximately 25% less intracellular inositol; purified ISYNA1 was not inhibited at that concentration. Condition category: machinery_impairment nutrient_topic: Inositol research collection; topical membership is not evidence of a direct dietary effect. plain_language: The effect depended on the cellular setting rather than direct inhibition of the isolated enzyme. organism: Human protein expressed in bacteria and yeast tissue_or_cell_type: Purified enzyme; yeast cultures experimental_model: Recombinant human enzyme and complementation of yeast ino1 deletion limitations: Purified-enzyme and yeast results do not establish supplement effects or a human dietary deficiency threshold. exposure: Substrate, NAD+, cation and valproate experiments evidence_span: {"source_cache": "artifacts/inositol-research/15024000.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5ab3a8eda77989c3e4a681b4a971fb7e969c285d3e5c8e41bc31713a7f88c9ac", "start_char": 0, "end_char": 1427, "text_sha256": "5ab3a8eda77989c3e4a681b4a971fb7e969c285d3e5c8e41bc31713a7f88c9ac"} [ino-p15024000] Human 1-D-myo-inositol-3-phosphate synthase is functional in yeast. (2004). https://pubmed.ncbi.nlm.nih.gov/15024000/ DOI: 10.1074/jbc.m312078200
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Gain- and loss-of-function experiments supported redundant contributions of ISYNA1 synthesis and SLC5A3 transport to intracellular inositol and AML-cell fitness.

    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/inositol-research/34531253.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e709021b8916a9b38a3a52f092732c2b587c55247c0bd9bd3f96438e74ad4b27", "start_char": 0, "end_char": 1431, "text_sha256": "e709021b8916a9b38a3a52f092732c2b587c55247c0bd9bd3f96438e74ad4b27"}
    experimental_model
    Genetic screening, gain/loss of function and patient sample profiling
    exposure
    SLC5A3/ISYNA1 perturbation
    limitations
    Restricted to an epigenetically defined subset; no evidence that dietary inositol restriction treats leukemia.
    nutrient_topic
    Inositol research collection; topical membership is not evidence of a direct dietary effect. · Inositol (stereoisomer family)
    organism
    Human AML cells and in vivo leukemia models
    plain_language
    Restoring synthesis can remove dependence on the same import route.
    primary_references
    [ino-p34531253] SLC5A3-Dependent Myo-inositol Auxotrophy in Acute Myeloid Leukemia. (2022). https://pubmed.ncbi.nlm.nih.gov/34531253/ DOI: 10.1158/2159-8290.cd-20-1849
    tissue_or_cell_type
    Acute myeloid leukemia
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Inositol: synthesis, signaling, mineral interactions and conditional deficiency (2026-09-17) · lines 418–429

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Genetic screening, gain/loss of function and patient sample profiling · source_derived_draft · unverified_draft

    ### ino-aml-redundancy Gain- and loss-of-function experiments supported redundant contributions of ISYNA1 synthesis and SLC5A3 transport to intracellular inositol and AML-cell fitness. Condition category: machinery_impairment nutrient_topic: Inositol research collection; topical membership is not evidence of a direct dietary effect. plain_language: Restoring synthesis can remove dependence on the same import route. organism: Human AML cells and in vivo leukemia models tissue_or_cell_type: Acute myeloid leukemia experimental_model: Genetic screening, gain/loss of function and patient sample profiling limitations: Restricted to an epigenetically defined subset; no evidence that dietary inositol restriction treats leukemia. exposure: SLC5A3/ISYNA1 perturbation evidence_span: {"source_cache": "artifacts/inositol-research/34531253.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e709021b8916a9b38a3a52f092732c2b587c55247c0bd9bd3f96438e74ad4b27", "start_char": 0, "end_char": 1431, "text_sha256": "e709021b8916a9b38a3a52f092732c2b587c55247c0bd9bd3f96438e74ad4b27"} [ino-p34531253] SLC5A3-Dependent Myo-inositol Auxotrophy in Acute Myeloid Leukemia. (2022). https://pubmed.ncbi.nlm.nih.gov/34531253/ DOI: 10.1158/2159-8290.cd-20-1849
    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