Component
Kir4.1/Kir5.1 heteromeric potassium channel
Basolateral channel containing KCNJ10 and KCNJ16; distinct from Kir4.1 homomers.
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.
Where it participates (unsigned role)
Adult renal Kir4.1 deletion depolarized DCT cells and abolished their voltage response to plasma potassium.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- cross_nutrient
- Potassium conductance is needed to regulate apical sodium/chloride transport.
- evidence_location
- Abstract and Discussion; DCT patch-clamp experiments.
- experimental_model
- Inducible adult kidney-specific Kcnj10 deletion
- limitations
- Genetic loss is not dietary deficiency; Kir5.1 participation was not directly deleted in this study.
- nutrient_topic
- Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
- organism
- Mus musculus
- plain_language
- Without Kir4.1, DCT cells lose the electrical response used to sense potassium.
- primary_references
- [cuevas-2017-kir4-sensing] Potassium Sensing by Renal Distal Tubules Requires Kir4.1 (2017). https://pmc.ncbi.nlm.nih.gov/articles/PMC5461801/ DOI: 10.1681/ASN.2016090935
- tissue_or_cell_type
- DCT basolateral membrane
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 190–201
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Inducible adult kidney-specific Kcnj10 deletion · source_derived_draft · unverified_draft
### renal-kir4-loss-disables-sensing Adult renal Kir4.1 deletion depolarized DCT cells and abolished their voltage response to plasma potassium. Condition category: machinery_impairment nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Without Kir4.1, DCT cells lose the electrical response used to sense potassium. organism: Mus musculus tissue_or_cell_type: DCT basolateral membrane experimental_model: Inducible adult kidney-specific Kcnj10 deletion limitations: Genetic loss is not dietary deficiency; Kir5.1 participation was not directly deleted in this study. cross_nutrient: Potassium conductance is needed to regulate apical sodium/chloride transport. evidence_location: Abstract and Discussion; DCT patch-clamp experiments. [cuevas-2017-kir4-sensing] Potassium Sensing by Renal Distal Tubules Requires Kir4.1 (2017). https://pmc.ncbi.nlm.nih.gov/articles/PMC5461801/ DOI: 10.1681/ASN.2016090935
Complete structured claim and evidenceKcnj16-null mice failed to change NCC abundance/phosphorylation with high- or low-K diets despite persistent Kir4.1 conductance.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- cross_nutrient
- Defective K sensing prevents appropriate sodium/chloride transporter adjustment.
- evidence_location
- Results and primary abstract; dietary electrophysiology and NCC assays.
- experimental_model
- Kir5.1 knockout with high/low K diets
- limitations
- Kir4.1 homomer conductance increases; this differs from Kir4.1 deletion.
- nutrient_topic
- Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
- organism
- Mus musculus
- plain_language
- The Kir5.1 partner allows this potassium channel system to adjust sodium transport when intake changes.
- primary_references
- [wang-2019-kir5-sensing] Deletion of Kir5.1 Impairs Renal Ability to Excrete Potassium during Increased Dietary Potassium Intake (2019). https://pmc.ncbi.nlm.nih.gov/articles/PMC6683724/ DOI: 10.1681/ASN.2019010025
- tissue_or_cell_type
- DCT
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 203–214
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Kir5.1 knockout with high/low K diets · source_derived_draft · unverified_draft
### renal-kir5-loss-prevents-diet-ncc-response Kcnj16-null mice failed to change NCC abundance/phosphorylation with high- or low-K diets despite persistent Kir4.1 conductance. Condition category: machinery_impairment nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The Kir5.1 partner allows this potassium channel system to adjust sodium transport when intake changes. organism: Mus musculus tissue_or_cell_type: DCT experimental_model: Kir5.1 knockout with high/low K diets limitations: Kir4.1 homomer conductance increases; this differs from Kir4.1 deletion. cross_nutrient: Defective K sensing prevents appropriate sodium/chloride transporter adjustment. evidence_location: Results and primary abstract; dietary electrophysiology and NCC assays. [wang-2019-kir5-sensing] Deletion of Kir5.1 Impairs Renal Ability to Excrete Potassium during Increased Dietary Potassium Intake (2019). https://pmc.ncbi.nlm.nih.gov/articles/PMC6683724/ DOI: 10.1681/ASN.2019010025
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.