Component

SLC5A3 (human SMIT1)

SLC5A3 (human SMIT1). 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. Gain- and loss-of-function experiments supported redundant contributions of ISYNA1 synthesis and SLC5A3 transport to intracellular inositol and AML-cell fitness.

    ISYNA1 (human inositol-3-phosphate synthase 1) → SLC5A3 (human SMIT1) source_derived_draftungraded
    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

  2. ISYNA1 transcriptional silencing characterized SLC5A3-dependent AML lines and produced an inositol auxotrophy.

    ISYNA1 transcriptional silencing → SLC5A3 (human SMIT1) source_derived_draftungraded
    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
    When a cell loses its synthesis route, the import route can become essential.
    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 405–416

    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-silencing ISYNA1 transcriptional silencing characterized SLC5A3-dependent AML lines and produced an inositol auxotrophy. Condition category: machinery_impairment nutrient_topic: Inositol research collection; topical membership is not evidence of a direct dietary effect. plain_language: When a cell loses its synthesis route, the import route can become essential. 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