Component

Mouse calcium-sensing receptor / Casr

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

6 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. The reported Casr knockout abolished rapid strontium-associated ERK1/2 phosphorylation in primary mouse osteoblasts.

    Mouse calcium-sensing receptor / Casr → Rapid ERK phosphorylation after strontium in mouse osteoblasts source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary full text, publicly accessible Methods and results
    experimental_model
    Mouse calvarial cells; exon-4-disrupted Casr model; SrCl2/sodium-ranelate mixture at 100:1, expressed as Sr2+ concentration.
    limitations
    Genotype and assay-specific finding; other response branches persisted.
    nutrient_topic
    Strontium collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Strontium
    plain_language
    One signaling branch requires the receptor in this model.
    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 86–92

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse calvarial cells; exon-4-disrupted Casr model; SrCl2/sodium-ranelate mixture at 100:1, expressed as Sr2+ concentration. · source_derived_draft · unverified_draft

    ## strontium-casr-knockout-erk One signaling branch requires the receptor in this model. The reported Casr knockout abolished rapid strontium-associated ERK1/2 phosphorylation in primary mouse osteoblasts. Model: Mouse calvarial cells; exon-4-disrupted Casr model; SrCl2/sodium-ranelate mixture at 100:1, expressed as Sr2+ concentration. Limitations: Genotype and assay-specific finding; other response branches persisted. Evidence access: Primary full text, publicly accessible Methods and results 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

  2. Pretreatment with NPS2390 largely antagonized ranelate-associated proliferation and mineralization in mouse MC3T3-E1 cells.

    Mouse calcium-sensing receptor / Casr → Strontium-associated MC3T3-E1 proliferation and mineralization source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary abstract
    experimental_model
    Mouse osteoblast-line pharmacological experiment.
    limitations
    NPS2390 is not a receptor-specific genetic deletion; later knockout experiments retain some responses.
    nutrient_topic
    Strontium collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Strontium
    plain_language
    A receptor inhibitor reduced the response in this culture model.
    primary_references
    The Calcium-sensing Receptor (CaR) is involved in strontium ranelate-induced osteoblast differentiation and mineralization. · 2010 · https://pubmed.ncbi.nlm.nih.gov/20560105/ · DOI 10.1055/s-0030-1255091
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Strontium: calcium interactions, cellular mechanisms and mineralization (2026-09-19) · lines 78–84

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse osteoblast-line pharmacological experiment. · source_derived_draft · unverified_draft

    ## strontium-mouse-casr-block A receptor inhibitor reduced the response in this culture model. Pretreatment with NPS2390 largely antagonized ranelate-associated proliferation and mineralization in mouse MC3T3-E1 cells. Model: Mouse osteoblast-line pharmacological experiment. Limitations: NPS2390 is not a receptor-specific genetic deletion; later knockout experiments retain some responses. Evidence access: Primary abstract The Calcium-sensing Receptor (CaR) is involved in strontium ranelate-induced osteoblast differentiation and mineralization. · 2010 · https://pubmed.ncbi.nlm.nih.gov/20560105/ · DOI 10.1055/s-0030-1255091
    Complete structured claim and evidence

  3. CaSR knockout abolished the phenylalanine-evoked calcium response in primary mouse I cells and prevented the normal stimulatory CCK response; responses to KCl and tryptone were preserved.

    Mouse calcium-sensing receptor / Casr → Mouse primary intestinal I-cell CCK secretion source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary abstract
    experimental_model
    CaSR-null compared with wild-type primary mouse intestinal I cells.
    limitations
    This is receptor failure, not phenylalanine or calcium dietary deficiency.
    nutrient_topic
    L-Phenylalanine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Phenylalanine
    plain_language
    Removing one sensor disables that route without disabling every secretion trigger.
    primary_references
    The extracellular calcium-sensing receptor is required for cholecystokinin secretion in response to L-phenylalanine in acutely isolated intestinal I cells. · 2011 · https://pubmed.ncbi.nlm.nih.gov/21252045/ · DOI 10.1152/ajpgi.00342.2010
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    L-Phenylalanine: transport, protein synthesis, cofactor recycling and cross-nutrient mechanisms (2026-09-19) · lines 286–292

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · CaSR-null compared with wild-type primary mouse intestinal I cells. · source_derived_draft · unverified_draft

    ## l-phenylalanine-casr-loss Removing one sensor disables that route without disabling every secretion trigger. CaSR knockout abolished the phenylalanine-evoked calcium response in primary mouse I cells and prevented the normal stimulatory CCK response; responses to KCl and tryptone were preserved. Model: CaSR-null compared with wild-type primary mouse intestinal I cells. Limitations: This is receptor failure, not phenylalanine or calcium dietary deficiency. Evidence access: Primary abstract The extracellular calcium-sensing receptor is required for cholecystokinin secretion in response to L-phenylalanine in acutely isolated intestinal I cells. · 2011 · https://pubmed.ncbi.nlm.nih.gov/21252045/ · DOI 10.1152/ajpgi.00342.2010
    Complete structured claim and evidence

Where it participates (unsigned role)

  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

  2. Strontium increased replication in both wild-type and Casr-knockout mouse osteoblasts despite loss of the rapid ERK response in knockout cells.

    Strontium ion / Sr2+ → Replication of Casr-knockout mouse osteoblasts source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract and accessible full-text Methods
    experimental_model
    Same primary mouse-cell study and defined SrCl2/ranelate mixture.
    limitations
    Does not identify the alternative sensor or establish universal CaSR independence.
    nutrient_topic
    Strontium collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Strontium
    plain_language
    Losing one receptor branch did not remove every growth response.
    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

    Strontium: calcium interactions, cellular mechanisms and mineralization (2026-09-19) · lines 94–100

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Same primary mouse-cell study and defined SrCl2/ranelate mixture. · source_derived_draft · unverified_draft

    ## strontium-casr-independent-growth Losing one receptor branch did not remove every growth response. Strontium increased replication in both wild-type and Casr-knockout mouse osteoblasts despite loss of the rapid ERK response in knockout cells. Model: Same primary mouse-cell study and defined SrCl2/ranelate mixture. Limitations: Does not identify the alternative sensor or establish universal CaSR independence. Evidence access: Primary abstract and accessible full-text Methods 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

  3. L-phenylalanine stimulated CaSR-dependent calcium signaling and CCK release in primary mouse duodenal I cells; CCK responses were greater at 2.5 than at 1.26 mM extracellular calcium.

    L-Phenylalanine → Mouse primary intestinal I-cell CCK secretion source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Primary mouse I cells; stereoselective L- versus D-phenylalanine responses.
    limitations
    Cell assay responses do not establish that calcium supplements enhance satiety in humans.
    nutrient_topic
    L-Phenylalanine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Phenylalanine
    plain_language
    Gut amino-acid sensing can depend on both the amino acid and calcium.
    primary_references
    The extracellular calcium-sensing receptor is required for cholecystokinin secretion in response to L-phenylalanine in acutely isolated intestinal I cells. · 2011 · https://pubmed.ncbi.nlm.nih.gov/21252045/ · DOI 10.1152/ajpgi.00342.2010

    L-Phenylalanine: transport, protein synthesis, cofactor recycling and cross-nutrient mechanisms (2026-09-19) · lines 278–284

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Primary mouse I cells; stereoselective L- versus D-phenylalanine responses. · source_derived_draft · unverified_draft

    ## l-phenylalanine-casr-cck Gut amino-acid sensing can depend on both the amino acid and calcium. L-phenylalanine stimulated CaSR-dependent calcium signaling and CCK release in primary mouse duodenal I cells; CCK responses were greater at 2.5 than at 1.26 mM extracellular calcium. Model: Primary mouse I cells; stereoselective L- versus D-phenylalanine responses. Limitations: Cell assay responses do not establish that calcium supplements enhance satiety in humans. Evidence access: Primary abstract The extracellular calcium-sensing receptor is required for cholecystokinin secretion in response to L-phenylalanine in acutely isolated intestinal I cells. · 2011 · https://pubmed.ncbi.nlm.nih.gov/21252045/ · DOI 10.1152/ajpgi.00342.2010
    Complete structured claim and evidence

In the sources

Preserved passages that mention this component, quoted exactly. Open one to read it in context.

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