Component
SUR1 K719A variant
SUR1 K719A variant; interpretation depends on linked experimental context.
1 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
SUR1 K719A or K1384M substitution impaired MgADP potentiation of cloned KATP currents.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- cross_nutrient
- A machinery defect interrupts magnesium-nucleotide regulation without demonstrating ion deficiency.
- experimental_model
- Mutant versus wild-type Xenopus patches.
- limitations
- Engineered substitutions are not evidence of dietary K or Mg deficiency.
- nutrient_topic
- Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
- organism
- Xenopus expression system
- plain_language
- Damaged nucleotide machinery can disrupt potassium-channel regulation.
- primary_references
- [gribble-1997-sur1] The essential role of the Walker A motifs of SUR1 in K-ATP channel activation by Mg-ADP and diazoxide (1997). https://pmc.ncbi.nlm.nih.gov/articles/PMC1169713/ DOI: 10.1093/emboj/16.6.1145
- tissue_or_cell_type
- Oocyte membrane
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 822–832
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mutant versus wild-type Xenopus patches. · source_derived_draft · unverified_draft
### k-sur1-mutations-mgadp SUR1 K719A or K1384M substitution impaired MgADP potentiation of cloned KATP currents. Condition category: machinery_impairment nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Damaged nucleotide machinery can disrupt potassium-channel regulation. organism: Xenopus expression system tissue_or_cell_type: Oocyte membrane experimental_model: Mutant versus wild-type Xenopus patches. limitations: Engineered substitutions are not evidence of dietary K or Mg deficiency. cross_nutrient: A machinery defect interrupts magnesium-nucleotide regulation without demonstrating ion deficiency. [gribble-1997-sur1] The essential role of the Walker A motifs of SUR1 in K-ATP channel activation by Mg-ADP and diazoxide (1997). https://pmc.ncbi.nlm.nih.gov/articles/PMC1169713/ DOI: 10.1093/emboj/16.6.1145
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.