Component

Human calcium/calmodulin-dependent protein kinase kinase 2 / CAMKK2

Context-specific entity; species, compartment and exposure are stated on each claim.

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 acts on it

  1. Under cysteine-deficient conditions, CARS promoted AMPK association with CaMKK2 and CaMKK2-dependent AMPK phosphorylation.

    Human cytosolic cysteinyl-tRNA synthetase / CARS1 → Human calcium/calmodulin-dependent protein kinase kinase 2 / CAMKK2 source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    evidence_access
    Primary abstract and indexed primary figure descriptions
    experimental_model
    Human 293T and cancer-cell experimental program.
    limitations
    CaMKK2 identity does not by itself show dietary calcium depletion or calcium-supplement rescue.
    nutrient_topic
    L-Cysteine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Cysteine
    plain_language
    The sensing protein helped bring a kinase and its target together.
    primary_references
    CARS senses cysteine deprivation to activate AMPK for cell survival. · 2021 · https://pubmed.ncbi.nlm.nih.gov/34472622/ · DOI 10.15252/embj.2021108028
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    L-Cysteine: sulfur allocation, redox supply and cross-nutrient mechanisms (2026-09-19) · lines 140–146

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human 293T and cancer-cell experimental program. · source_derived_draft · unverified_draft

    ## l-cysteine-cars-camkk2-bridge The sensing protein helped bring a kinase and its target together. Under cysteine-deficient conditions, CARS promoted AMPK association with CaMKK2 and CaMKK2-dependent AMPK phosphorylation. Model: Human 293T and cancer-cell experimental program. Limitations: CaMKK2 identity does not by itself show dietary calcium depletion or calcium-supplement rescue. Evidence access: Primary abstract and indexed primary figure descriptions CARS senses cysteine deprivation to activate AMPK for cell survival. · 2021 · https://pubmed.ncbi.nlm.nih.gov/34472622/ · DOI 10.15252/embj.2021108028
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Sodium butyrate promoted store-operated calcium entry and activated the CaMKK-beta/AMPK pathway during Caco-2 tight-junction reassembly, without the change being explained by ATP concentration.

    Butyrate → Store-operated calcium entry in butyrate-exposed Caco-2 cells source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Human Caco-2 calcium-switch model.
    limitations
    This does not show that dietary calcium or magnesium supplementation improves the response.
    nutrient_topic
    Butyrate collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Butyrate
    plain_language
    Calcium signaling helped connect butyrate to barrier repair.
    primary_references
    Sodium Butyrate Promotes Reassembly of Tight Junctions in Caco-2 Monolayers Involving Inhibition of MLCK/MLC2 Pathway and Phosphorylation of PKCβ2. · 2016 · https://pubmed.ncbi.nlm.nih.gov/27735862/ · DOI 10.3390/ijms17101696

    Butyrate: microbial production, fuel use, signaling and nutrient interactions (2026-09-19) · lines 270–276

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human Caco-2 calcium-switch model. · source_derived_draft · unverified_draft

    ## butyrate-calcium-soce Calcium signaling helped connect butyrate to barrier repair. Sodium butyrate promoted store-operated calcium entry and activated the CaMKK-beta/AMPK pathway during Caco-2 tight-junction reassembly, without the change being explained by ATP concentration. Model: Human Caco-2 calcium-switch model. Limitations: This does not show that dietary calcium or magnesium supplementation improves the response. Evidence access: Primary abstract Sodium Butyrate Promotes Reassembly of Tight Junctions in Caco-2 Monolayers Involving Inhibition of MLCK/MLC2 Pathway and Phosphorylation of PKCβ2. · 2016 · https://pubmed.ncbi.nlm.nih.gov/27735862/ · DOI 10.3390/ijms17101696
    Complete structured claim and evidence

  2. Blocking AMPK activation increased cell death under cysteine-deficient conditions in the tested cultures.

    Human AMP-activated protein kinase complexes → Survival of cysteine-starved human cells source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    evidence_access
    Primary abstract
    experimental_model
    Human-cell nutrient-withdrawal experiments with AMPK-pathway perturbation.
    limitations
    This is an adaptive response under culture deprivation, not evidence that chronic dietary deprivation is beneficial.
    nutrient_topic
    L-Cysteine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Cysteine
    plain_language
    The response to scarcity helped cells survive it.
    primary_references
    CARS senses cysteine deprivation to activate AMPK for cell survival. · 2021 · https://pubmed.ncbi.nlm.nih.gov/34472622/ · DOI 10.15252/embj.2021108028
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    L-Cysteine: sulfur allocation, redox supply and cross-nutrient mechanisms (2026-09-19) · lines 148–154

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human-cell nutrient-withdrawal experiments with AMPK-pathway perturbation. · source_derived_draft · unverified_draft

    ## l-cysteine-ampk-adaptation The response to scarcity helped cells survive it. Blocking AMPK activation increased cell death under cysteine-deficient conditions in the tested cultures. Model: Human-cell nutrient-withdrawal experiments with AMPK-pathway perturbation. Limitations: This is an adaptive response under culture deprivation, not evidence that chronic dietary deprivation is beneficial. Evidence access: Primary abstract CARS senses cysteine deprivation to activate AMPK for cell survival. · 2021 · https://pubmed.ncbi.nlm.nih.gov/34472622/ · DOI 10.15252/embj.2021108028
    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