Component
Protein phosphatase 1 catalytic subunit alpha
Canonical protein; experimental species, state, expression context and nutritional dependence are specified per claim.
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
PP1A directly bound the NCC regulatory terminus and dephosphorylated NCC; high extracellular K enhanced their association in MDCKI-hNCC cells.
Experimental context and source evidence
- cross_nutrient
- K-dependent phosphatase engagement reduces the activation signal of the Na/Cl transporter.
- evidence_location
- Figure 6A-C.
- experimental_model
- Purified binding/phosphatase assays and MDCKI-hNCC cells
- limitations
- Binding/activity assays do not by themselves quantify sodium transport in humans.
- nutrient_topic
- Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
- organism
- Recombinant proteins; Canis lupus familiaris cell line expressing human NCC
- plain_language
- Potassium can increase contact between NCC and an enzyme that removes its phosphate signal.
- primary_references
- [grimm-2023-pp1a-ncc] Dietary potassium stimulates Ppp1Ca-Ppp1r1a dephosphorylation of kidney NaCl cotransporter and reduces blood pressure (2023). https://www.jci.org/articles/view/158498 DOI: 10.1172/JCI158498
- tissue_or_cell_type
- Cell-free and kidney-derived cells
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 268–279
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Purified binding/phosphatase assays and MDCKI-hNCC cells · source_derived_draft · unverified_draft
### renal-pp1a-dephosphorylates-ncc PP1A directly bound the NCC regulatory terminus and dephosphorylated NCC; high extracellular K enhanced their association in MDCKI-hNCC cells. Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Potassium can increase contact between NCC and an enzyme that removes its phosphate signal. organism: Recombinant proteins; Canis lupus familiaris cell line expressing human NCC tissue_or_cell_type: Cell-free and kidney-derived cells experimental_model: Purified binding/phosphatase assays and MDCKI-hNCC cells limitations: Binding/activity assays do not by themselves quantify sodium transport in humans. cross_nutrient: K-dependent phosphatase engagement reduces the activation signal of the Na/Cl transporter. evidence_location: Figure 6A-C. [grimm-2023-pp1a-ncc] Dietary potassium stimulates Ppp1Ca-Ppp1r1a dephosphorylation of kidney NaCl cotransporter and reduces blood pressure (2023). https://www.jci.org/articles/view/158498 DOI: 10.1172/JCI158498
Complete structured claim and evidence
Where it participates (unsigned role)
After high-K dietary adaptation, DCT-specific constitutively active SPAK mice reduced NCC phosphorylation despite persistent kinase activation.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- cross_nutrient
- Dietary K adjusts the balance controlling Na/Cl transporter activation.
- evidence_location
- Figure 1; Figures 4-5; Discussion.
- experimental_model
- Four-day dietary K loading in CA-SPAK mice
- limitations
- Response required higher plasma K than controls; not a general claim that kinase state is irrelevant.
- nutrient_topic
- Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
- organism
- Mus musculus
- plain_language
- With adaptation, the phosphate-removing response can overcome a continuously active kinase.
- primary_references
- [grimm-2023-pp1a-ncc] Dietary potassium stimulates Ppp1Ca-Ppp1r1a dephosphorylation of kidney NaCl cotransporter and reduces blood pressure (2023). https://www.jci.org/articles/view/158498 DOI: 10.1172/JCI158498
- tissue_or_cell_type
- DCT
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 281–292
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Four-day dietary K loading in CA-SPAK mice · source_derived_draft · unverified_draft
### renal-k-adaptation-overcomes-active-spak After high-K dietary adaptation, DCT-specific constitutively active SPAK mice reduced NCC phosphorylation despite persistent kinase activation. Condition category: machinery_impairment nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: With adaptation, the phosphate-removing response can overcome a continuously active kinase. organism: Mus musculus tissue_or_cell_type: DCT experimental_model: Four-day dietary K loading in CA-SPAK mice limitations: Response required higher plasma K than controls; not a general claim that kinase state is irrelevant. cross_nutrient: Dietary K adjusts the balance controlling Na/Cl transporter activation. evidence_location: Figure 1; Figures 4-5; Discussion. [grimm-2023-pp1a-ncc] Dietary potassium stimulates Ppp1Ca-Ppp1r1a dephosphorylation of kidney NaCl cotransporter and reduces blood pressure (2023). https://www.jci.org/articles/view/158498 DOI: 10.1172/JCI158498
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.