Component
Human ENaC beta-subunit P616L variant as numbered in the 1995 study
Human ENaC beta-subunit P616L variant as numbered in the 1995 study. Species, exposure and limitations are retained in each linked 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.
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
The beta-subunit P616L mutant increased amiloride-sensitive sodium current 8.8-fold versus normal subunits in oocytes.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_span
- {"source_cache": "artifacts/sodium-research/8524790.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "31f8bb4c6f32108b9d6042db6ec60ed8c77b21af322621a2cb0fd9c2aa7236a1", "start_char": 0, "end_char": 1598, "text_sha256": "31f8bb4c6f32108b9d6042db6ec60ed8c77b21af322621a2cb0fd9c2aa7236a1"}
- experimental_model
- Human kindred analysis and oocyte channel-expression comparison
- exposure
- P616L as numbered in the paper
- limitations
- Gain-of-function genetic disease; no implication that this mutation is caused by salt intake.
- nutrient_topic
- Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
- organism
- Human variant in Xenopus oocytes
- plain_language
- A mutation can make sodium entry excessive even without a defective sodium supply.
- primary_references
- [sodium-p8524790] A de novo missense mutation of the beta subunit of the epithelial sodium channel causes hypertension and Liddle syndrome, identifying a proline-rich segment critical for regulation of channel activity. (1995). https://pubmed.ncbi.nlm.nih.gov/8524790/ DOI: 10.1073/pnas.92.25.11495
- tissue_or_cell_type
- ENaC beta-subunit regulatory tail
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 954–965
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human kindred analysis and oocyte channel-expression comparison · source_derived_draft · unverified_draft
### sodium-liddle-current The beta-subunit P616L mutant increased amiloride-sensitive sodium current 8.8-fold versus normal subunits in oocytes. Condition category: machinery_impairment nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: A mutation can make sodium entry excessive even without a defective sodium supply. organism: Human variant in Xenopus oocytes tissue_or_cell_type: ENaC beta-subunit regulatory tail experimental_model: Human kindred analysis and oocyte channel-expression comparison limitations: Gain-of-function genetic disease; no implication that this mutation is caused by salt intake. exposure: P616L as numbered in the paper evidence_span: {"source_cache": "artifacts/sodium-research/8524790.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "31f8bb4c6f32108b9d6042db6ec60ed8c77b21af322621a2cb0fd9c2aa7236a1", "start_char": 0, "end_char": 1598, "text_sha256": "31f8bb4c6f32108b9d6042db6ec60ed8c77b21af322621a2cb0fd9c2aa7236a1"} [sodium-p8524790] A de novo missense mutation of the beta subunit of the epithelial sodium channel causes hypertension and Liddle syndrome, identifying a proline-rich segment critical for regulation of channel activity. (1995). https://pubmed.ncbi.nlm.nih.gov/8524790/ DOI: 10.1073/pnas.92.25.11495
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.