ArticleThe Journal of general physiology2017
On the effect of hyperaldosteronism-inducing mutations in Na/K pumps.
Article in The Journal of general physiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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.
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.
Who cites it
23 citing papers in PubMed, 27 citations in OpenAlex.
- On the mechanism of hypomagnesemia with treatment-resistant seizures caused by variants of the Na+,K+-ATPase α1 subunit (ATP1A1).The Journal of general physiology · 2026Article
- Association of the RecurrentNeurology. Genetics · 2025Article
- Article
- ATP1A1-linked diseases require a malfunctioning protein product from one allele.Biochimica et biophysica acta. Molecular cell research · 2024Article
- Primary aldosteronism: molecular medicine meets public health.Nature reviews. Nephrology · 2023Review
- Cation leak through the ATP1A3 pump causes spasticity and intellectual disability.Brain : a journal of neurology · 2023Article
- The phenotypic spectrum of pathogenic ATP1A1 variants expands: the novel p.P600R substitution causes demyelinating Charcot-Marie-Tooth disease.Journal of neurology · 2023Article
- The NaeLife · 2022Article
- Structure and function of HNature communications · 2022Article
- Disease mutations of human α3 NaPNAS nexus · 2022Article
- Role of a conserved ion-binding site tyrosine in ion selectivity of the Na+/K+ pump.The Journal of general physiology · 2022Article
- Diseases caused by mutations in the NaAmerican journal of physiology. Cell physiology · 2021Review
- Displacement of the NaProceedings of the National Academy of Sciences of the United States of America · 2021Article
- FXYD protein isoforms differentially modulate human Na/K pump function.The Journal of general physiology · 2020Article
- Transient Electrical Currents Mediated by the NaBiophysical journal · 2020Review
- Distinct effects of Q925 mutation on intracellular and extracellular NaScientific reports · 2019Article
- Na/K Pump Mutations Associated with Primary Hyperaldosteronism Cause Loss of Function.Biochemistry · 2019Article
- Genotype-structure-phenotype relationships diverge in paralogsNeurology. Genetics · 2019Review
- Functional consequences of the CAPOS mutation E818K of NaThe Journal of biological chemistry · 2019Article
- Article
Corrections and comments
- Commented on by
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Primary aldosteronism, a condition in which too much aldosterone is produced and that leads to hypertension, is often initiated by an aldosterone-producing adenoma within the zona glomerulosa of the adrenal cortex. Somatic mutations of ATP1A1, encoding the Na/K pump α1 subunit, have been found in these adenomas. It has been proposed that a passive inward current transported by several of these mutant pumps is a "gain-of-function" activity that produces membrane depolarization and concomitant increases in aldosterone production. Here, we investigate whether the inward current through mutant Na/K pumps is large enough to induce depolarization of the cells that harbor them. We first investigate inward currents induced by these mutations in
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.