Component

SECISBP2 / SBP2

SECIS-binding protein involved in selenocysteine insertion during translation.

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. SECISBP2 deficiency compromises a required component of SECIS-dependent selenocysteine decoding.

    SECISBP2 / SBP2 → UGA recoding source_derived_draftsource_reported: Human genetic disease and biochemical mechanism as reported in the supplied source; unverified synthesis.
    Experimental context and source evidence
    availability_state
    Rare genetic SECISBP2 deficiency, distinct from inadequate dietary selenium.
    experimental_scope
    Rare human genetic disorder and biochemical role of SECIS-dependent recoding.
    limitations
    Growth, muscle, and reproductive findings in genetic disease are not direct phenocopies of ordinary dietary deficiency. Adequate intake does not define machinery function.
    trigger_kind
    machinery_impairment

    Selenium deficiency: a mechanism-first reference · lines 35–41

    Supplied selenium deficiency reference · supports · Supplied reference; verify the primary study and experimental context. · source_derived_draft · unverified_draft

    Sec-tRNA^[Ser]Sec ↓ eEFSec ribosome reaches UGA ↓ SECIS + SECISBP2/SBP2 machinery ↓ SELENOCYSTEINE INSERTED

    Selenium deficiency: a mechanism-first reference · lines 83–83

    Supplied selenium deficiency reference · supports · Supplied reference; verify the primary study and experimental context. · source_derived_draft · unverified_draft

    Layer 2 — SECIS-dependent translation. SECIS structure, SECISBP2/SBP2 interactions, eEFSec, ribosomal context, and other RNA-binding proteins influence recoding efficiency.

    Selenium deficiency: a mechanism-first reference · lines 497–509

    Supplied selenium deficiency reference · supports · Supplied reference; verify the primary study and experimental context. · source_derived_draft · unverified_draft

    Rare genetic disorders help show what happens when parts of selenoprotein biology fail despite adequate dietary selenium. Gene / protein Disorder or molecular role Selected phenotype / implication SECISBP2 (SBP2) SECISBP2 deficiency Abnormal thyroid-hormone profile, growth and muscle phenotypes, male infertility and other multisystem effects
    Complete structured claim and evidence

  2. Human SECISBP2 deficiency is associated with an abnormal thyroid-hormone profile.

    SECISBP2 / SBP2 → Local thyroid-hormone metabolism source_derived_draftsource_reported: Human genetic disease and biochemical mechanism as reported in the supplied source; unverified synthesis.
    Experimental context and source evidence
    availability_state
    Rare genetic SECISBP2 deficiency, distinct from inadequate dietary selenium.
    experimental_scope
    Rare human genetic disorder and biochemical role of SECIS-dependent recoding.
    limitations
    Growth, muscle, and reproductive findings in genetic disease are not direct phenocopies of ordinary dietary deficiency. Adequate intake does not define machinery function.
    trigger_kind
    machinery_impairment

    Selenium deficiency: a mechanism-first reference · lines 505–509

    Supplied selenium deficiency reference · supports · Supplied reference; verify the primary study and experimental context. · source_derived_draft · unverified_draft

    SECISBP2 (SBP2) SECISBP2 deficiency Abnormal thyroid-hormone profile, growth and muscle phenotypes, male infertility and other multisystem effects
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Fibroblasts from affected siblings with a recessive SECISBP2 defect had reduced DIO2 activity; linkage did not map the defect to DIO2 itself.

    Patients with recessive SECISBP2 defects → DIO2 source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    Selenium-incorporation machinery is required for hormone-processing selenoproteins; this is not dietary selenium deficiency.
    evidence_locator
    Primary abstract
    evidence_spans
    [{"source_document": "artifacts/iodine-metabolism-sources/16228000.json", "source_field": "resultList.result[0].abstractText", "start_char": 0, "end_char": 1084}]
    experimental_model
    Two human families with recessive SECISBP2 variants; patient fibroblast enzyme assays and linkage analysis
    exposure
    Inherited SECISBP2 variants; no dietary deprivation exposure.
    limitations
    Abstract-only; variant-specific kinetics and dietary rescue were not established.
    nutrient_topic
    Iodine research collection; topical membership is not evidence of a direct dietary effect. · Iodine
    organism
    Homo sapiens
    plain_language
    A defect in selenium-incorporation machinery can impair thyroid-hormone processing even when the deiodinase gene is not the cause.
    primary_references
    [i-met-16228000] Mutations in SECISBP2 result in abnormal thyroid hormone metabolism. (2005). https://pubmed.ncbi.nlm.nih.gov/16228000/ DOI: 10.1038/ng1654
    tissue_or_cell_type
    Patient fibroblasts
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Iodine: thyroid hormone production, deficiency, excess and nutrient interactions (2026-09-17) · lines 1099–1112

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Two human families with recessive SECISBP2 variants; patient fibroblast enzyme assays and linkage analysis · source_derived_draft · unverified_draft

    ### i-met-secisbp2-fibroblast-dio2 Fibroblasts from affected siblings with a recessive SECISBP2 defect had reduced DIO2 activity; linkage did not map the defect to DIO2 itself. Condition category: machinery_impairment nutrient_topic: Iodine research collection; topical membership is not evidence of a direct dietary effect. plain_language: A defect in selenium-incorporation machinery can impair thyroid-hormone processing even when the deiodinase gene is not the cause. organism: Homo sapiens tissue_or_cell_type: Patient fibroblasts experimental_model: Two human families with recessive SECISBP2 variants; patient fibroblast enzyme assays and linkage analysis limitations: Abstract-only; variant-specific kinetics and dietary rescue were not established. exposure: Inherited SECISBP2 variants; no dietary deprivation exposure. cross_nutrient: Selenium-incorporation machinery is required for hormone-processing selenoproteins; this is not dietary selenium deficiency. evidence_locator: Primary abstract evidence_spans: [{"source_document": "artifacts/iodine-metabolism-sources/16228000.json", "source_field": "resultList.result[0].abstractText", "start_char": 0, "end_char": 1084}] [i-met-16228000] Mutations in SECISBP2 result in abnormal thyroid hormone metabolism. (2005). https://pubmed.ncbi.nlm.nih.gov/16228000/ DOI: 10.1038/ng1654
    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