Component

Mouse phosphatidylinositol 3-kinase complexes (isoform unresolved)

Mouse phosphatidylinositol 3-kinase complexes (isoform unresolved). 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

Where it participates (unsigned role)

  1. Chromium co-treatment increased GLUT4 levels relative to the iron-only condition, alongside higher PI3K and Akt phosphorylation ratios.

    Chromium(III) picolinate / CrPic → Mouse glucose transporter 4 / Slc2a4 source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/chromium-research/37156991.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e5b7952975edd461bc01f9a4389588789a7d1b7dedf56fb97270051092ae6cda", "start_char": 0, "end_char": 1621, "text_sha256": "e5b7952975edd461bc01f9a4389588789a7d1b7dedf56fb97270051092ae6cda"}
    experimental_model
    C2C12 cell experiments with supporting database pathway analysis
    exposure
    Chromium picolinate, ferric ammonium citrate and combination
    limitations
    Pathway databases generate hypotheses. Co-changing ROS and signaling measurements do not alone establish a unique causal sequence; no human iron-overload treatment was tested.
    nutrient_topic
    Chromium research collection; topical membership is not evidence of a direct dietary effect. · Chromium
    organism
    Mouse C2C12 skeletal-muscle cells
    plain_language
    The glucose transporter and measured signaling steps were less suppressed.
    primary_references
    [chromium-p37156991] Antagonizing Effects of Chromium Against Iron-Decreased Glucose Uptake by Regulating ROS-Mediated PI3K/Akt/GLUT4 Signaling Pathway in C2C12. (2024). https://pubmed.ncbi.nlm.nih.gov/37156991/ DOI: 10.1007/s12011-023-03695-z
    tissue_or_cell_type
    Cellular glucose uptake, ROS assays and signaling proteins

    Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 796–807

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · C2C12 cell experiments with supporting database pathway analysis · source_derived_draft · unverified_draft

    ### chromium-iron-cell-glut4 Chromium co-treatment increased GLUT4 levels relative to the iron-only condition, alongside higher PI3K and Akt phosphorylation ratios. Condition category: normal nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The glucose transporter and measured signaling steps were less suppressed. organism: Mouse C2C12 skeletal-muscle cells tissue_or_cell_type: Cellular glucose uptake, ROS assays and signaling proteins experimental_model: C2C12 cell experiments with supporting database pathway analysis limitations: Pathway databases generate hypotheses. Co-changing ROS and signaling measurements do not alone establish a unique causal sequence; no human iron-overload treatment was tested. exposure: Chromium picolinate, ferric ammonium citrate and combination evidence_span: {"source_cache": "artifacts/chromium-research/37156991.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e5b7952975edd461bc01f9a4389588789a7d1b7dedf56fb97270051092ae6cda", "start_char": 0, "end_char": 1621, "text_sha256": "e5b7952975edd461bc01f9a4389588789a7d1b7dedf56fb97270051092ae6cda"} [chromium-p37156991] Antagonizing Effects of Chromium Against Iron-Decreased Glucose Uptake by Regulating ROS-Mediated PI3K/Akt/GLUT4 Signaling Pathway in C2C12. (2024). https://pubmed.ncbi.nlm.nih.gov/37156991/ DOI: 10.1007/s12011-023-03695-z
    Complete structured claim and evidence

  2. LY294002 reversed nasunin-associated protection and worsened t-BHP cytotoxicity.

    LY294002 → MC3T3-E1 osteoblast-like cell viability source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/nasunin-research/bone2016.publisher-abstract.txt", "locator": "Primary publisher abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "83d6dc95bb4cccd5028a3908a5a44639274f59f18e1cea4b13f6133b9fe726dc", "start_char": 0, "end_char": 1187, "text_sha256": "83d6dc95bb4cccd5028a3908a5a44639274f59f18e1cea4b13f6133b9fe726dc"}
    experimental_model
    Oxidant-challenged osteoblast-like cells with pharmacological pathway inhibition
    exposure
    Purified trans-nasunin pretreatment 0.1 nM-1 micromolar; t-BHP 250 micromolar for 3 h; redox/function experiments at 1 nM
    limitations
    Cell-line protection does not establish bone-density or fracture benefits in humans. PI3K inhibition supports pathway involvement, not direct nasunin binding.
    nutrient_topic
    Nasunin research collection; topical membership is not evidence of a direct dietary effect. · Nasunin
    organism
    Mouse MC3T3-E1 cells
    plain_language
    The pathway must remain functional for this observed protection.
    primary_references
    [nasunin-pbone2016] Nasunin, a new player in the field of osteoblast protection against oxidative stress (2016). https://air.unimi.it/handle/2434/378237 DOI: 10.1016/j.jff.2016.03.007
    tissue_or_cell_type
    Survival, differentiation markers, redox state and Akt signaling
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Nasunin: identity, redox chemistry and nutrient connections (2026-09-17) · lines 406–417

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Oxidant-challenged osteoblast-like cells with pharmacological pathway inhibition · source_derived_draft · unverified_draft

    ### nasunin-bone-pi3k-dependence LY294002 reversed nasunin-associated protection and worsened t-BHP cytotoxicity. Condition category: machinery_impairment nutrient_topic: Nasunin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The pathway must remain functional for this observed protection. organism: Mouse MC3T3-E1 cells tissue_or_cell_type: Survival, differentiation markers, redox state and Akt signaling experimental_model: Oxidant-challenged osteoblast-like cells with pharmacological pathway inhibition limitations: Cell-line protection does not establish bone-density or fracture benefits in humans. PI3K inhibition supports pathway involvement, not direct nasunin binding. exposure: Purified trans-nasunin pretreatment 0.1 nM-1 micromolar; t-BHP 250 micromolar for 3 h; redox/function experiments at 1 nM evidence_span: {"source_cache": "artifacts/nasunin-research/bone2016.publisher-abstract.txt", "locator": "Primary publisher abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "83d6dc95bb4cccd5028a3908a5a44639274f59f18e1cea4b13f6133b9fe726dc", "start_char": 0, "end_char": 1187, "text_sha256": "83d6dc95bb4cccd5028a3908a5a44639274f59f18e1cea4b13f6133b9fe726dc"} [nasunin-pbone2016] Nasunin, a new player in the field of osteoblast protection against oxidative stress (2016). https://air.unimi.it/handle/2434/378237 DOI: 10.1016/j.jff.2016.03.007
    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