Component

Protein phosphatase 1 regulatory inhibitor subunit 1A

Canonical protein; experimental species, state, expression context and nutritional dependence are specified per claim.

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.

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.

Recorded relationships

Where it participates (unsigned role)

  1. After high-K dietary adaptation, DCT-specific constitutively active SPAK mice reduced NCC phosphorylation despite persistent kinase activation.

    Potassium → NCC phosphorylation source_derived_draftungraded
    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

In the sources

Preserved passages that mention this component, quoted exactly. Open one to read it in context.

    This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.

    Evidence, AI assistance and curation standards