Component

ENaC surface abundance

ENaC abundance at the apical plasma membrane, distinct from cleavage or open probability.

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

What acts on it

  1. SGK-dependent Nedd4-2 phosphorylation reduced its ENaC interaction and increased ENaC surface expression in oocytes.

    SGK-phosphorylated NEDD4L → ENaC surface abundance source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    Higher sodium-channel availability can support the secretory machinery used for K balance.
    evidence_location
    Figures 3-5; interaction and anti-FLAG surface-labeling experiments.
    experimental_model
    Oocyte binding, current and surface-labeling assays
    limitations
    Molecular sufficiency does not establish exclusive control in intact kidneys.
    nutrient_topic
    Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
    organism
    Xenopus laevis
    plain_language
    Phosphorylation weakens the sodium-channel removal signal, leaving more channels at the surface.
    primary_references
    [debonneville-2001-sgk-nedd4] Phosphorylation of Nedd4-2 by Sgk1 regulates epithelial Na(+) channel cell surface expression (2001). https://pubmed.ncbi.nlm.nih.gov/11742982/ DOI: 10.1093/emboj/20.24.7052
    tissue_or_cell_type
    Oocytes

    Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 421–432

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Oocyte binding, current and surface-labeling assays · source_derived_draft · unverified_draft

    ### renal-phospho-nedd4l-releases-enac SGK-dependent Nedd4-2 phosphorylation reduced its ENaC interaction and increased ENaC surface expression in oocytes. Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Phosphorylation weakens the sodium-channel removal signal, leaving more channels at the surface. organism: Xenopus laevis tissue_or_cell_type: Oocytes experimental_model: Oocyte binding, current and surface-labeling assays limitations: Molecular sufficiency does not establish exclusive control in intact kidneys. cross_nutrient: Higher sodium-channel availability can support the secretory machinery used for K balance. evidence_location: Figures 3-5; interaction and anti-FLAG surface-labeling experiments. [debonneville-2001-sgk-nedd4] Phosphorylation of Nedd4-2 by Sgk1 regulates epithelial Na(+) channel cell surface expression (2001). https://pubmed.ncbi.nlm.nih.gov/11742982/ DOI: 10.1093/emboj/20.24.7052
    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