Component
Ser256-phosphorylated AQP2
AQP2 phosphorylated at serine 256.
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 acts on it
Dietary potassium restriction reduced Ser256-phosphorylated AQP2 in cortical and medullary collecting ducts of both male and female mice.
Experimental context and source evidence
- availability_state
- nutrient_deficiency Imported condition classification; unverified.
- endpoint
- Dietary potassium restriction reduced Ser256-phosphorylated AQP2 in cortical and medullary collecting ducts of both male and female mice.
- experimental-exposure
- Male and female C57BL/6J mice exposed to graded potassium restriction for eight days; water-balance and collecting-duct signaling measurements.
- experimental_model
- Male and female C57BL/6J mice exposed to graded potassium restriction for eight days; water-balance and collecting-duct signaling measurements.
- limitations
- Sex and segment influenced severity; this does not establish a universal human plasma-potassium threshold or a unique responsible kinase.
- nutrient_topic
- Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
- organism
- Mus musculus
- plain_language
- The channel activation/trafficking state changed even where total protein loss was less marked.
- primary_references
- [al-qusairi-2021-vasopressin] Rapid development of vasopressin resistance in dietary K+ deficiency (2021). https://pubmed.ncbi.nlm.nih.gov/33749322/ DOI: 10.1152/ajprenal.00655.2020
- tissue_or_cell_type
- cortical and medullary collecting duct
- trigger_kind
- nutrient_deficiency Imported condition classification; unverified.
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1412–1423
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Male and female C57BL/6J mice exposed to graded potassium restriction for eight days; water-balance and collecting-duct signaling measurements. · source_derived_draft · unverified_draft
### k-restriction-lowers-aqp2-ser256 Dietary potassium restriction reduced Ser256-phosphorylated AQP2 in cortical and medullary collecting ducts of both male and female mice. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The channel activation/trafficking state changed even where total protein loss was less marked. organism: Mus musculus tissue_or_cell_type: cortical and medullary collecting duct experimental_model: Male and female C57BL/6J mice exposed to graded potassium restriction for eight days; water-balance and collecting-duct signaling measurements. limitations: Sex and segment influenced severity; this does not establish a universal human plasma-potassium threshold or a unique responsible kinase. experimental-exposure: Male and female C57BL/6J mice exposed to graded potassium restriction for eight days; water-balance and collecting-duct signaling measurements. endpoint: Dietary potassium restriction reduced Ser256-phosphorylated AQP2 in cortical and medullary collecting ducts of both male and female mice. [al-qusairi-2021-vasopressin] Rapid development of vasopressin resistance in dietary K+ deficiency (2021). https://pubmed.ncbi.nlm.nih.gov/33749322/ DOI: 10.1152/ajprenal.00655.2020
Complete structured claim and evidence
Where it participates (unsigned role)
Principal-cell Atg7 deletion worsened urine-concentrating impairment during potassium depletion rather than rescuing it.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- endpoint
- Principal-cell Atg7 deletion worsened urine-concentrating impairment during potassium depletion rather than rescuing it.
- experimental-exposure
- Principal-cell Atg7 conditional knockout and floxed control mice on normal or potassium-free diet for two weeks.
- experimental_model
- Principal-cell Atg7 conditional knockout and floxed control mice on normal or potassium-free diet for two weeks.
- limitations
- Knockout already altered basal urine concentration and caused compensatory degradation changes; this is not evidence against every role for autophagy.
- nutrient_topic
- Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
- organism
- Mus musculus
- plain_language
- Blocking one protein-disposal pathway did not restore water balance; channel phosphorylation and localization still mattered.
- primary_references
- [kim-2019-atg7-aqp2] Atg7-dependent canonical autophagy regulates the degradation of aquaporin 2 in prolonged hypokalemia (2019). https://www.nature.com/articles/s41598-019-39702-4 DOI: 10.1038/s41598-019-39702-4
- tissue_or_cell_type
- collecting-duct principal cells
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1425–1436
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Principal-cell Atg7 conditional knockout and floxed control mice on normal or potassium-free diet for two weeks. · source_derived_draft · unverified_draft
### atg7-loss-worsens-hypokalemic-concentrating-defect Principal-cell Atg7 deletion worsened urine-concentrating impairment during potassium depletion rather than rescuing it. Condition category: machinery_impairment nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Blocking one protein-disposal pathway did not restore water balance; channel phosphorylation and localization still mattered. organism: Mus musculus tissue_or_cell_type: collecting-duct principal cells experimental_model: Principal-cell Atg7 conditional knockout and floxed control mice on normal or potassium-free diet for two weeks. limitations: Knockout already altered basal urine concentration and caused compensatory degradation changes; this is not evidence against every role for autophagy. experimental-exposure: Principal-cell Atg7 conditional knockout and floxed control mice on normal or potassium-free diet for two weeks. endpoint: Principal-cell Atg7 deletion worsened urine-concentrating impairment during potassium depletion rather than rescuing it. [kim-2019-atg7-aqp2] Atg7-dependent canonical autophagy regulates the degradation of aquaporin 2 in prolonged hypokalemia (2019). https://www.nature.com/articles/s41598-019-39702-4 DOI: 10.1038/s41598-019-39702-4
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.