Component

Mouse Akt protein family (isoform unresolved)

Mouse Akt protein family (isoform unresolved). Species, exposure and limitations are retained in each linked claim.

5 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. Pharmacological Akt inhibition abolished strontium protection against osteoblast apoptosis in the tested wild-type and Casr-knockout mouse cultures.

    Mouse Akt protein family (isoform unresolved) → Strontium-associated survival of mouse osteoblasts source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary abstract
    experimental_model
    Serum deprivation or IL-1beta/TNF-alpha challenge in mouse osteoblasts.
    limitations
    Pharmacological evidence; Akt isoform unresolved.
    nutrient_topic
    Strontium collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Strontium
    plain_language
    A downstream survival pathway remained necessary even when the receptor was absent.
    primary_references
    Calcium sensing receptor-dependent and receptor-independent activation of osteoblast replication and survival by strontium ranelate. · 2009 · https://pubmed.ncbi.nlm.nih.gov/20141614/ · DOI 10.1111/j.1582-4934.2009.00673.x
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Strontium: calcium interactions, cellular mechanisms and mineralization (2026-09-19) · lines 102–108

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Serum deprivation or IL-1beta/TNF-alpha challenge in mouse osteoblasts. · source_derived_draft · unverified_draft

    ## strontium-akt-survival A downstream survival pathway remained necessary even when the receptor was absent. Pharmacological Akt inhibition abolished strontium protection against osteoblast apoptosis in the tested wild-type and Casr-knockout mouse cultures. Model: Serum deprivation or IL-1beta/TNF-alpha challenge in mouse osteoblasts. Limitations: Pharmacological evidence; Akt isoform unresolved. Evidence access: Primary abstract Calcium sensing receptor-dependent and receptor-independent activation of osteoblast replication and survival by strontium ranelate. · 2009 · https://pubmed.ncbi.nlm.nih.gov/20141614/ · DOI 10.1111/j.1582-4934.2009.00673.x
    Complete structured claim and evidence

What acts on it

  1. Nasunin attenuated Akt phosphorylation in stimulated RAW264 cells.

    Nasunin → Mouse Akt protein family (isoform unresolved) source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/nasunin-research/28812425.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7a697b4eb979f1e6349bc79f4d2ed0d3994de51dfed777a71fb04740819eeabf", "start_char": 0, "end_char": 1094, "text_sha256": "7a697b4eb979f1e6349bc79f4d2ed0d3994de51dfed777a71fb04740819eeabf"}
    experimental_model
    LPS-stimulated macrophage experiments
    exposure
    Dose-dependent nasunin treatment; exact dose/time not reported in indexed abstract
    limitations
    These measurements do not prove direct binding to Akt, p38, NF-kappa-B or NOS2; reduced NOS2 expression is not direct enzyme inhibition. Response is LPS/cell-context dependent.
    nutrient_topic
    Nasunin research collection; topical membership is not evidence of a direct dietary effect. · Nasunin
    organism
    Mouse RAW264 macrophages
    plain_language
    The direction applies to this inflammatory setting.
    primary_references
    [nasunin-p28812425] Nasunin inhibits the lipopolysaccharide-induced pro-inflammatory mediator production in RAW264 mouse macrophages by suppressing ROS-mediated activation of PI3 K/Akt/NF-κB and p38 signaling pathways. (2017). https://pubmed.ncbi.nlm.nih.gov/28812425/ DOI: 10.1080/09168451.2017.1362973
    tissue_or_cell_type
    Inflammatory mediator secretion and signaling

    Nasunin: identity, redox chemistry and nutrient connections (2026-09-17) · lines 276–287

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · LPS-stimulated macrophage experiments · source_derived_draft · unverified_draft

    ### nasunin-akt-macrophage Nasunin attenuated Akt phosphorylation in stimulated RAW264 cells. Condition category: normal nutrient_topic: Nasunin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The direction applies to this inflammatory setting. organism: Mouse RAW264 macrophages tissue_or_cell_type: Inflammatory mediator secretion and signaling experimental_model: LPS-stimulated macrophage experiments limitations: These measurements do not prove direct binding to Akt, p38, NF-kappa-B or NOS2; reduced NOS2 expression is not direct enzyme inhibition. Response is LPS/cell-context dependent. exposure: Dose-dependent nasunin treatment; exact dose/time not reported in indexed abstract evidence_span: {"source_cache": "artifacts/nasunin-research/28812425.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7a697b4eb979f1e6349bc79f4d2ed0d3994de51dfed777a71fb04740819eeabf", "start_char": 0, "end_char": 1094, "text_sha256": "7a697b4eb979f1e6349bc79f4d2ed0d3994de51dfed777a71fb04740819eeabf"} [nasunin-p28812425] Nasunin inhibits the lipopolysaccharide-induced pro-inflammatory mediator production in RAW264 mouse macrophages by suppressing ROS-mediated activation of PI3 K/Akt/NF-κB and p38 signaling pathways. (2017). https://pubmed.ncbi.nlm.nih.gov/28812425/ DOI: 10.1080/09168451.2017.1362973
    Complete structured claim and evidence

  2. Nasunin prevented the challenge-associated loss of Akt phosphorylation.

    trans-Nasunin → Mouse Akt protein family (isoform unresolved) source_derived_draftungraded
    Experimental context and source evidence
    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
    Here the protective response preserved signaling rather than suppressing it.
    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

    Nasunin: identity, redox chemistry and nutrient connections (2026-09-17) · lines 393–404

    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-akt Nasunin prevented the challenge-associated loss of Akt phosphorylation. Condition category: normal nutrient_topic: Nasunin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Here the protective response preserved signaling rather than suppressing it. 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

Where it participates (unsigned role)

  1. GPX1-overexpressing mice showed reduced insulin-stimulated receptor phosphorylation in liver and Akt phosphorylation in liver and soleus.

    Mouse Gpx1 overexpression genotype → Mouse insulin receptor / Insr source_derived_draftungraded
    Experimental context and source evidence
    curation_topic
    selenium · Selenium
    experimental_condition
    Wild-type mice on the same diet GPX1 overexpression · Mouse Gpx1 overexpression genotype Condition belongs to the full experimental contrast; do not separate a joint intervention.
    experimental_contrast
    {"intervention": "GPX1 overexpression", "comparator": "Wild-type mice on the same diet", "endpoint": "Insulin-stimulated phosphorylation", "effect_direction": "decrease", "combination": "single", "conditions": [{"entity_slug": "mouse-gpx1-overexpression", "state": "GPX1 overexpression"}]} Explicit extracted experimental comparison; source-derived draft.
    experimental_model
    Male transgenic mice; selenium-adequate 0.4 mg/kg diet, ages 8 to 24 weeks
    limitations
    Overexpression experiment, not dietary selenium excess. Excess ROS quenching is a proposed explanation rather than a measured universal mechanism.
    primary_references
    McClung et al. 2004; DOI:10.1073/pnas.0308096101; PMID:15184668; https://pmc.ncbi.nlm.nih.gov/articles/PMC428436/

    Diabetes cascade: targeted primary-source supplement · lines 30–30

    See claim-local references; curated paraphrases reviewed 2026-09-20. · supports · Male transgenic mice; selenium-adequate 0.4 mg/kg diet, ages 8 to 24 weeks · source_derived_draft · unverified_draft

    GPX1-overexpressing mice showed reduced insulin-stimulated receptor phosphorylation in liver and Akt phosphorylation in liver and soleus. Model: Male transgenic mice; selenium-adequate 0.4 mg/kg diet, ages 8 to 24 weeks. Limits: Overexpression experiment, not dietary selenium excess. Excess ROS quenching is a proposed explanation rather than a measured universal mechanism. Primary reference: McClung et al. 2004; DOI:10.1073/pnas.0308096101; PMID:15184668; https://pmc.ncbi.nlm.nih.gov/articles/PMC428436/
    Complete structured claim and evidence

  2. 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

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.

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