Component

Mouse glycogen synthase kinase 3 beta / Gsk3b

Context-specific entity; species, compartment and exposure are stated on each 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 acts on it

  1. Lithium depletion increased GSK3beta expression and activation-associated signals in mouse brain.

    Mouse cortical lithium availability → Mouse glycogen synthase kinase 3 beta / Gsk3b source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    evidence_access
    Primary full text
    experimental_model
    Mouse neurons, oligodendrocytes and microglial analyses.
    limitations
    Not a universal linear relation between serum lithium and enzyme activity.
    nutrient_topic
    Lithium collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Lithium
    plain_language
    The enzyme connects availability to downstream responses.
    primary_references
    Lithium deficiency and the onset of Alzheimer's disease. · 2025 · https://pubmed.ncbi.nlm.nih.gov/40770094/ · DOI 10.1038/s41586-025-09335-x
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Lithium: metal-sensitive enzymes, transport and cross-nutrient mechanisms (2026-09-19) · lines 456–462

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse neurons, oligodendrocytes and microglial analyses. · source_derived_draft · unverified_draft

    ## lithium-depletion-gsk3 The enzyme connects availability to downstream responses. Lithium depletion increased GSK3beta expression and activation-associated signals in mouse brain. Model: Mouse neurons, oligodendrocytes and microglial analyses. Limitations: Not a universal linear relation between serum lithium and enzyme activity. Evidence access: Primary full text Lithium deficiency and the onset of Alzheimer's disease. · 2025 · https://pubmed.ncbi.nlm.nih.gov/40770094/ · DOI 10.1038/s41586-025-09335-x
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Lithium disrupted a beta-arrestin2–Akt–PP2A complex and altered Akt/GSK3 signaling in mice.

    Lithium ion (Li+) → Mouse beta-arrestin2–Akt–PP2A signaling complex source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Mouse pharmacology and biochemical complex assays.
    limitations
    A second pathway alongside direct enzyme inhibition, not a complete explanation of mood stabilization.
    nutrient_topic
    Lithium collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Lithium
    plain_language
    Lithium can change how signaling proteins assemble.
    primary_references
    A beta-arrestin 2 signaling complex mediates lithium action on behavior. · 2008 · https://pubmed.ncbi.nlm.nih.gov/18191226/ · DOI 10.1016/j.cell.2007.11.041

    Lithium: metal-sensitive enzymes, transport and cross-nutrient mechanisms (2026-09-19) · lines 192–198

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse pharmacology and biochemical complex assays. · source_derived_draft · unverified_draft

    ## lithium-arrestin-complex Lithium can change how signaling proteins assemble. Lithium disrupted a beta-arrestin2–Akt–PP2A complex and altered Akt/GSK3 signaling in mice. Model: Mouse pharmacology and biochemical complex assays. Limitations: A second pathway alongside direct enzyme inhibition, not a complete explanation of mood stabilization. Evidence access: Primary abstract A beta-arrestin 2 signaling complex mediates lithium action on behavior. · 2008 · https://pubmed.ncbi.nlm.nih.gov/18191226/ · DOI 10.1016/j.cell.2007.11.041
    Complete structured claim and evidence

  2. Arrb2 knockout prevented the reported lithium effects on Akt/GSK3 signaling and associated mouse behaviors.

    Mouse beta-arrestin 2 / Arrb2 → Mouse beta-arrestin2–Akt–PP2A signaling complex source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary abstract
    experimental_model
    Mouse Arrb2 knockout comparison.
    limitations
    Does not abolish every molecular lithium effect.
    nutrient_topic
    Lithium collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Lithium
    plain_language
    Removing the scaffold removed this lithium response.
    primary_references
    A beta-arrestin 2 signaling complex mediates lithium action on behavior. · 2008 · https://pubmed.ncbi.nlm.nih.gov/18191226/ · DOI 10.1016/j.cell.2007.11.041
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Lithium: metal-sensitive enzymes, transport and cross-nutrient mechanisms (2026-09-19) · lines 200–206

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse Arrb2 knockout comparison. · source_derived_draft · unverified_draft

    ## lithium-arrestin-loss Removing the scaffold removed this lithium response. Arrb2 knockout prevented the reported lithium effects on Akt/GSK3 signaling and associated mouse behaviors. Model: Mouse Arrb2 knockout comparison. Limitations: Does not abolish every molecular lithium effect. Evidence access: Primary abstract A beta-arrestin 2 signaling complex mediates lithium action on behavior. · 2008 · https://pubmed.ncbi.nlm.nih.gov/18191226/ · DOI 10.1016/j.cell.2007.11.041
    Complete structured claim and evidence

  3. Lithium-associated period lengthening accompanied altered SCN GSK3 expression and phosphorylation in mice.

    Lithium ion (Li+) → Mouse locomotor circadian period source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Mouse locomotor monitoring and suprachiasmatic-nucleus assays.
    limitations
    Association does not establish that GSK3 is the sole circadian target.
    nutrient_topic
    Lithium collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Lithium
    plain_language
    A brain clock and its signaling proteins changed together.
    primary_references
    Effect of lithium on the circadian rhythms of locomotor activity and glycogen synthase kinase-3 protein expression in the mouse suprachiasmatic nuclei. · 2004 · https://pubmed.ncbi.nlm.nih.gov/15090054/ · DOI 10.1111/j.0953-816X.2004.03322.x

    Lithium: metal-sensitive enzymes, transport and cross-nutrient mechanisms (2026-09-19) · lines 256–262

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse locomotor monitoring and suprachiasmatic-nucleus assays. · source_derived_draft · unverified_draft

    ## lithium-clock-mouse A brain clock and its signaling proteins changed together. Lithium-associated period lengthening accompanied altered SCN GSK3 expression and phosphorylation in mice. Model: Mouse locomotor monitoring and suprachiasmatic-nucleus assays. Limitations: Association does not establish that GSK3 is the sole circadian target. Evidence access: Primary abstract Effect of lithium on the circadian rhythms of locomotor activity and glycogen synthase kinase-3 protein expression in the mouse suprachiasmatic nuclei. · 2004 · https://pubmed.ncbi.nlm.nih.gov/15090054/ · DOI 10.1111/j.0953-816X.2004.03322.x
    Complete structured claim and evidence

  4. GSK3 inhibition restored amyloid uptake/degradation in microglia from lithium-depleted mice.

    CHIR99021 → Mouse microglial amyloid uptake and degradation source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    evidence_access
    Primary full text
    experimental_model
    CHIR99021 and companion PF-04802367 rescue assays.
    limitations
    Inhibitor rescue supports partial mediation, not a single-target explanation.
    nutrient_topic
    Lithium collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Lithium
    plain_language
    Blocking the downstream enzyme helped test the proposed chain.
    primary_references
    Lithium deficiency and the onset of Alzheimer's disease. · 2025 · https://pubmed.ncbi.nlm.nih.gov/40770094/ · DOI 10.1038/s41586-025-09335-x
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Lithium: metal-sensitive enzymes, transport and cross-nutrient mechanisms (2026-09-19) · lines 488–494

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · CHIR99021 and companion PF-04802367 rescue assays. · source_derived_draft · unverified_draft

    ## lithium-gsk3-rescue Blocking the downstream enzyme helped test the proposed chain. GSK3 inhibition restored amyloid uptake/degradation in microglia from lithium-depleted mice. Model: CHIR99021 and companion PF-04802367 rescue assays. Limitations: Inhibitor rescue supports partial mediation, not a single-target explanation. Evidence access: Primary full text Lithium deficiency and the onset of Alzheimer's disease. · 2025 · https://pubmed.ncbi.nlm.nih.gov/40770094/ · DOI 10.1038/s41586-025-09335-x
    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