Component
Mouse CALHM1 / Calhm1
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.
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.
Other things that act on it
Enzymes, hormones, genes, and other components with a recorded effect. These are not nutrients, so they do not count toward the arrows above. Each finding names the chapter that recorded it.
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.
What it acts on
Calhm1 knockout reduced taste-evoked ATP release without eliminating taste-cell excitability to the stimuli.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_access
- Primary abstract
- experimental_model
- Mouse taste-bud knockout physiology.
- limitations
- The later CALHM3 work refines the channel composition; CALHM1 is not treated as the sole physiological subunit.
- nutrient_topic
- Monosodium Glutamate (MSG) collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Monosodium L-glutamate
- plain_language
- A cell can detect a stimulus yet fail to transmit its message.
- primary_references
- CALHM1 ion channel mediates purinergic neurotransmission of sweet, bitter and umami tastes. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23467090/ · DOI 10.1038/nature11906
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Monosodium Glutamate (MSG): taste, gut sensing, exposure and cross-nutrient mechanisms (2026-09-20) · lines 114–120
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse taste-bud knockout physiology. · source_derived_draft · unverified_draft
## monosodium-glutamate-calhm1-release A cell can detect a stimulus yet fail to transmit its message. Calhm1 knockout reduced taste-evoked ATP release without eliminating taste-cell excitability to the stimuli. Model: Mouse taste-bud knockout physiology. Limitations: The later CALHM3 work refines the channel composition; CALHM1 is not treated as the sole physiological subunit. Evidence access: Primary abstract CALHM1 ion channel mediates purinergic neurotransmission of sweet, bitter and umami tastes. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23467090/ · DOI 10.1038/nature11906
Complete structured claim and evidence
What acts on it
CALHM3 coassembly with CALHM1 conferred rapid voltage-dependent ATP-release-channel gating; the study connected this complex to type II taste-cell physiology.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Heterologous channel experiments and mouse taste-cell physiology.
- limitations
- Functional coassembly is recorded without treating the historical proposed stoichiometry as a universal structural assignment.
- nutrient_topic
- Monosodium Glutamate (MSG) collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Monosodium L-glutamate
- plain_language
- Two separately stored subunits form the output channel.
- primary_references
- CALHM3 Is Essential for Rapid Ion Channel-Mediated Purinergic Neurotransmission of GPCR-Mediated Tastes. · 2018 · https://pubmed.ncbi.nlm.nih.gov/29681531/ · DOI 10.1016/j.neuron.2018.03.043
Monosodium Glutamate (MSG): taste, gut sensing, exposure and cross-nutrient mechanisms (2026-09-20) · lines 122–128
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Heterologous channel experiments and mouse taste-cell physiology. · source_derived_draft · unverified_draft
## monosodium-glutamate-calhm3-channel Two separately stored subunits form the output channel. CALHM3 coassembly with CALHM1 conferred rapid voltage-dependent ATP-release-channel gating; the study connected this complex to type II taste-cell physiology. Model: Heterologous channel experiments and mouse taste-cell physiology. Limitations: Functional coassembly is recorded without treating the historical proposed stoichiometry as a universal structural assignment. Evidence access: Primary abstract CALHM3 Is Essential for Rapid Ion Channel-Mediated Purinergic Neurotransmission of GPCR-Mediated Tastes. · 2018 · https://pubmed.ncbi.nlm.nih.gov/29681531/ · DOI 10.1016/j.neuron.2018.03.043
Complete structured claim and evidence
Where it participates (unsigned role)
Calhm3 deletion abolished taste-evoked ATP release and disrupted GPCR-mediated taste perception in mice.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_access
- Primary abstract
- experimental_model
- Mouse knockout experiments.
- limitations
- Shares investigators with the CALHM1 study; no human deficiency threshold follows.
- nutrient_topic
- Monosodium Glutamate (MSG) collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Monosodium L-glutamate
- plain_language
- Intact upstream sensing cannot compensate for a missing release channel.
- primary_references
- CALHM3 Is Essential for Rapid Ion Channel-Mediated Purinergic Neurotransmission of GPCR-Mediated Tastes. · 2018 · https://pubmed.ncbi.nlm.nih.gov/29681531/ · DOI 10.1016/j.neuron.2018.03.043
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Monosodium Glutamate (MSG): taste, gut sensing, exposure and cross-nutrient mechanisms (2026-09-20) · lines 130–136
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse knockout experiments. · source_derived_draft · unverified_draft
## monosodium-glutamate-calhm3-loss Intact upstream sensing cannot compensate for a missing release channel. Calhm3 deletion abolished taste-evoked ATP release and disrupted GPCR-mediated taste perception in mice. Model: Mouse knockout experiments. Limitations: Shares investigators with the CALHM1 study; no human deficiency threshold follows. Evidence access: Primary abstract CALHM3 Is Essential for Rapid Ion Channel-Mediated Purinergic Neurotransmission of GPCR-Mediated Tastes. · 2018 · https://pubmed.ncbi.nlm.nih.gov/29681531/ · DOI 10.1016/j.neuron.2018.03.043
Complete structured claim and evidence
The events it takes part in
A mechanism often involves more than two components. These are the full events, with every participant and its role.
Situations it appears in
Low-supply and faulty-machinery situations recorded in the chapters where this component plays a part.
In the sources
Preserved passages that mention this component, quoted exactly. Open one to read it in context.
Open hypotheses
Proposed ideas that involve this component. They are labeled as hypotheses and do not change any recorded statement.
This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.