Component
Kir6.2-SUR1 ATP-sensitive potassium channel
Kir6.2-SUR1 ATP-sensitive potassium channel; interpretation depends on linked experimental context.
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 acts on it
MgADP potentiated cloned Kir6.2/SUR1 current through intact SUR1 nucleotide-binding machinery.
Experimental context and source evidence
- cross_nutrient
- MgADP supplies a magnesium-dependent regulatory input to potassium conductance.
- experimental_model
- Xenopus oocyte cloned-channel patches.
- limitations
- Heterologous channel biochemistry, not nutritional magnesium depletion.
- nutrient_topic
- Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
- organism
- Xenopus expression system
- plain_language
- Magnesium-bound ADP helps keep this potassium channel active.
- 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
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 810–820
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Xenopus oocyte cloned-channel patches. · source_derived_draft · unverified_draft
### k-mgadp-sur1-activation MgADP potentiated cloned Kir6.2/SUR1 current through intact SUR1 nucleotide-binding machinery. Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Magnesium-bound ADP helps keep this potassium channel active. organism: Xenopus expression system tissue_or_cell_type: Oocyte membrane experimental_model: Xenopus oocyte cloned-channel patches. limitations: Heterologous channel biochemistry, not nutritional magnesium depletion. cross_nutrient: MgADP supplies a magnesium-dependent regulatory input to potassium conductance. [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 evidenceSUR1 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
Where it participates (unsigned role)
Glucose metabolism closed resting potassium channels in cell-attached rat beta-cell recordings.
Experimental context and source evidence
- cross_nutrient
- Carbohydrate metabolism regulates a potassium conductance rather than proving potassium supplementation benefit.
- experimental_model
- Cell-attached patch recordings in isolated rat pancreatic beta cells; glucose and metabolism perturbation.
- limitations
- The experiment does not establish dietary potassium control of insulin secretion.
- nutrient_topic
- Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
- organism
- Rat
- plain_language
- The glucose fuel signal reduced potassium conductance.
- primary_references
- [ashcroft-1984-glucose] Glucose induces closure of single potassium channels in isolated rat pancreatic beta-cells (1984). https://www.nature.com/articles/312446a0 DOI: 10.1038/312446a0
- tissue_or_cell_type
- Pancreatic beta cells
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 774–784
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cell-attached patch recordings in isolated rat pancreatic beta cells; glucose and metabolism perturbation. · source_derived_draft · unverified_draft
### k-glucose-closes-beta-channel Glucose metabolism closed resting potassium channels in cell-attached rat beta-cell recordings. Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The glucose fuel signal reduced potassium conductance. organism: Rat tissue_or_cell_type: Pancreatic beta cells experimental_model: Cell-attached patch recordings in isolated rat pancreatic beta cells; glucose and metabolism perturbation. limitations: The experiment does not establish dietary potassium control of insulin secretion. cross_nutrient: Carbohydrate metabolism regulates a potassium conductance rather than proving potassium supplementation benefit. [ashcroft-1984-glucose] Glucose induces closure of single potassium channels in isolated rat pancreatic beta-cells (1984). https://www.nature.com/articles/312446a0 DOI: 10.1038/312446a0
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.