Evidence map›Paper›PMID 26772908›Full record

ReviewGene2016

Epithelial sodium channel (ENaC) family: Phylogeny, structure-function, tissue distribution, and associated inherited diseases.

Israel Hanukoglu, Aaron Hanukoglu

Open access · greenAbstract readReview
In one paragraph

Review in Gene, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 213 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
213citing papers in PubMed, 4 pooled it
20.7field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

213 citing papers in PubMed, 4 syntheses or guidelines pooled it, 402 citations in OpenAlex.

  1. A frameshift mutation in theMolecular medicine reports · 2024
    Pooled it
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  5. Trial
  6. Review
  7. From idiopathic pulmonary hemosiderosis to ENaC channelopathy: a novel SCNN1G mutation.American journal of respiratory and critical care medicine · 2026
    Article
  8. Article
  9. Article
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  13. Pathophysiology of homocysteine: insights into ion channel dysfunction.Pflugers Archiv : European journal of physiology · 2026
    Review
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  17. Article
  18. Article
  19. Article
  20. The scaffold protein IQGAP1 regulates the epithelial NaThe Journal of biological chemistry · 2025
    Article

153 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 2 institutions in 1 country.

Israel HanukogluLaboratory of Cell Biology, Faculty of Natural Sciences, Ariel University, Ariel, Israel. Electronic address: mbiochem@gmail.com.
Aaron HanukogluDivision of Pediatric Endocrinology, E. Wolfson Medical Center, Holon, Israel; Sackler School of Medicine, Tel-Aviv University, Tel Aviv, Israel.
Ariel University · ILWolfson Medical Center · IL

Funding

The Gene Wiki: Community intelligence applied to gene annotationR01GM089820 · NIGMS · SCRIPPS RESEARCH INSTITUTE, THE · PI SU, ANDREW I · 2010 to 2021
$5.2M
Canadian Institutes of Health Research MOP 97917NIGMS NIH HHS GM089820NIGMS NIH HHS R01 GM089820
6 · The paper itself

Abstract

The epithelial sodium channel (ENaC) is composed of three homologous subunits and allows the flow of Na(+) ions across high resistance epithelia, maintaining body salt and water homeostasis. ENaC dependent reabsorption of Na(+) in the kidney tubules regulates extracellular fluid (ECF) volume and blood pressure by modulating osmolarity. In multi-ciliated cells, ENaC is located in cilia and plays an essential role in the regulation of epithelial surface liquid volume necessary for cilial transport of mucus and gametes in the respiratory and reproductive tracts respectively. The subunits that form ENaC (named as alpha, beta, gamma and delta, encoded by genes SCNN1A, SCNN1B, SCNN1G, and SCNN1D) are members of the ENaC/Degenerin superfamily. The earliest appearance of ENaC orthologs is in the genomes of the most ancient vertebrate taxon, Cyclostomata (jawless vertebrates) including lampreys, followed by earliest representatives of Gnathostomata (jawed vertebrates) including cartilaginous sharks. Among Euteleostomi (bony vertebrates), Actinopterygii (ray finned-fishes) branch has lost ENaC genes. Yet, most animals in the Sarcopterygii (lobe-finned fish) branch including Tetrapoda, amphibians and amniotes (lizards, crocodiles, birds, and mammals), have four ENaC paralogs. We compared the sequences of ENaC orthologs from 20 species and established criteria for the identification of ENaC orthologs and paralogs, and their distinction from other members of the ENaC/Degenerin superfamily, especially ASIC family. Differences between ENaCs and ASICs are summarized in view of their physiological functions and tissue distributions. Structural motifs that are conserved throughout vertebrate ENaCs are highlighted. We also present a comparative overview of the genotype-phenotype relationships in inherited diseases associated with ENaC mutations, including multisystem pseudohypoaldosteronism (PHA1B), Liddle syndrome, cystic fibrosis-like disease and essential hypertension.

Indexed as

AnimalsCystic FibrosisEpithelial Sodium ChannelsEssential HypertensionHumansHypertensionMutationOrgan SpecificityPhylogenyProtein ConformationSodiumStructure-Activity RelationshipEpithelial Sodium ChannelsSodiumEpitheliaEvolutionIon channelsKidneyRenin–angiotensin–aldosterone systemTransmembrane proteins

Identifiers

PMID26772908
PMCPMC4756657
OpenAlexW2227999806

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.