Component
NEDD4-like E3 ubiquitin protein ligase
Canonical protein; experimental species, state, expression context and nutritional dependence are specified per claim.
3 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
Sgk1 phosphorylated Nedd4-2 at Ser444 and less strongly Ser338 in Xenopus constructs.
Experimental context and source evidence
- cross_nutrient
- This biochemical sodium-channel pathway contributes to the machinery for K handling.
- evidence_location
- Figure 2.
- experimental_model
- Expression, kinase-dead and site-mutant experiments
- limitations
- Residue numbers are construct/species-specific; nutritional K sensing was not tested.
- nutrient_topic
- Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
- organism
- Xenopus laevis
- plain_language
- SGK1 modifies the protein that normally restrains sodium channels.
- 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 408–419
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Expression, kinase-dead and site-mutant experiments · source_derived_draft · unverified_draft
### renal-sgk1-phosphorylates-nedd4l Sgk1 phosphorylated Nedd4-2 at Ser444 and less strongly Ser338 in Xenopus constructs. Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: SGK1 modifies the protein that normally restrains sodium channels. organism: Xenopus laevis tissue_or_cell_type: Oocytes experimental_model: Expression, kinase-dead and site-mutant experiments limitations: Residue numbers are construct/species-specific; nutritional K sensing was not tested. cross_nutrient: This biochemical sodium-channel pathway contributes to the machinery for K handling. evidence_location: Figure 2. [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
Where it participates (unsigned role)
SGK-dependent Nedd4-2 phosphorylation reduced its ENaC interaction and increased ENaC surface expression in oocytes.
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 evidenceRenal Sgk1 deletion blunted the early increase in urinary K excretion on high-K feeding, with hyperkalemia and reduced ENaC processing.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- cross_nutrient
- Impaired ENaC sodium-channel adaptation accompanies defective K clearance.
- evidence_location
- Results Figure 2; two-day versus five-day dietary comparison.
- experimental_model
- Inducible tubular deletion; two-day high-K citrate diet
- limitations
- Excretion approached controls after longer adaptation; ROMK apical localization increased rather than decreased.
- nutrient_topic
- Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
- organism
- Mus musculus
- plain_language
- Removing kidney SGK1 impairs the initial ability to clear a potassium load.
- primary_references
- [al-qusairi-2016-renal-sgk1] Renal tubular SGK1 deficiency causes impaired K+ excretion via loss of regulation of NEDD4-2/WNK1 and ENaC (2016). https://pmc.ncbi.nlm.nih.gov/articles/PMC5005279/ DOI: 10.1152/ajprenal.00002.2016
- tissue_or_cell_type
- Kidney tubules
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 434–445
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Inducible tubular deletion; two-day high-K citrate diet · source_derived_draft · unverified_draft
### renal-sgk1-loss-impairs-high-k-excretion Renal Sgk1 deletion blunted the early increase in urinary K excretion on high-K feeding, with hyperkalemia and reduced ENaC processing. Condition category: machinery_impairment nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Removing kidney SGK1 impairs the initial ability to clear a potassium load. organism: Mus musculus tissue_or_cell_type: Kidney tubules experimental_model: Inducible tubular deletion; two-day high-K citrate diet limitations: Excretion approached controls after longer adaptation; ROMK apical localization increased rather than decreased. cross_nutrient: Impaired ENaC sodium-channel adaptation accompanies defective K clearance. evidence_location: Results Figure 2; two-day versus five-day dietary comparison. [al-qusairi-2016-renal-sgk1] Renal tubular SGK1 deficiency causes impaired K+ excretion via loss of regulation of NEDD4-2/WNK1 and ENaC (2016). https://pmc.ncbi.nlm.nih.gov/articles/PMC5005279/ DOI: 10.1152/ajprenal.00002.2016
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.