Component
CaV1.1 R528H variant
CaV1.1 R528H variant; interpretation depends on linked experimental context.
2 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
R528H mouse fibers displayed anomalous inward current at resting potentials, supporting a voltage-sensor leak mechanism.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- experimental_model
- Knock-in mouse fiber voltage clamp.
- limitations
- The leak is not equivalent to the normal calcium-conducting pore.
- nutrient_topic
- Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
- organism
- Mouse
- plain_language
- An inherited calcium-channel variant added an abnormal leak.
- primary_references
- [wu-2012-hypopp] A calcium channel mutant mouse model of hypokalemic periodic paralysis (2012). https://pmc.ncbi.nlm.nih.gov/articles/PMC3533564/ DOI: 10.1172/JCI66091
- tissue_or_cell_type
- Skeletal muscle
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 751–760
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Knock-in mouse fiber voltage clamp. · source_derived_draft · unverified_draft
### k-hypopp-gating-pore R528H mouse fibers displayed anomalous inward current at resting potentials, supporting a voltage-sensor leak mechanism. Condition category: machinery_impairment nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: An inherited calcium-channel variant added an abnormal leak. organism: Mouse tissue_or_cell_type: Skeletal muscle experimental_model: Knock-in mouse fiber voltage clamp. limitations: The leak is not equivalent to the normal calcium-conducting pore. [wu-2012-hypopp] A calcium channel mutant mouse model of hypokalemic periodic paralysis (2012). https://pmc.ncbi.nlm.nih.gov/articles/PMC3533564/ DOI: 10.1172/JCI66091
Complete structured claim and evidenceAt 2 mM bath K, R528H muscle paradoxically depolarized and lost force while wild-type fibers hyperpolarized.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- cross_nutrient
- A calcium-channel genetic defect changes potassium sensitivity of sodium-dependent muscle excitability.
- experimental_model
- 4.75 to 2 mM K challenge; mouse muscle recordings.
- limitations
- Sex/genotype influenced susceptibility; no general dietary-paralysis claim.
- nutrient_topic
- Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
- organism
- Mouse
- plain_language
- The same low-potassium exposure acted differently with inherited channel impairment.
- primary_references
- [wu-2012-hypopp] A calcium channel mutant mouse model of hypokalemic periodic paralysis (2012). https://pmc.ncbi.nlm.nih.gov/articles/PMC3533564/ DOI: 10.1172/JCI66091
- tissue_or_cell_type
- Skeletal muscle
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 762–772
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · 4.75 to 2 mM K challenge; mouse muscle recordings. · source_derived_draft · unverified_draft
### k-hypopp-low-k-depolarization At 2 mM bath K, R528H muscle paradoxically depolarized and lost force while wild-type fibers hyperpolarized. Condition category: machinery_impairment nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The same low-potassium exposure acted differently with inherited channel impairment. organism: Mouse tissue_or_cell_type: Skeletal muscle experimental_model: 4.75 to 2 mM K challenge; mouse muscle recordings. limitations: Sex/genotype influenced susceptibility; no general dietary-paralysis claim. cross_nutrient: A calcium-channel genetic defect changes potassium sensitivity of sodium-dependent muscle excitability. [wu-2012-hypopp] A calcium channel mutant mouse model of hypokalemic periodic paralysis (2012). https://pmc.ncbi.nlm.nih.gov/articles/PMC3533564/ DOI: 10.1172/JCI66091
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.