Evidence map›Paper›PMID 25904388›Full record

ReviewPflugers Archiv : European journal of physiology2015

A unifying mechanism for WNK kinase regulation of sodium-chloride cotransporter.

Chou-Long Huang, Chih-Jen Cheng

Abstract readReview
In one paragraph

Review in Pflugers Archiv : European journal of physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
–field-weighted citation impact
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

19 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Differential roles of WNK4 in regulation of NCC in vivo.American journal of physiology. Renal physiology · 2018
    Article
  11. OSR1 regulates a subset of inward rectifier potassium channels via a binding motif variant.Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  12. WNK Kinases in Development and Disease.Current topics in developmental biology · 2017
    Review
  13. Potassium Homeostasis, Oxidative Stress, and Human Disease.International journal of clinical and experimental physiology · 2017
    Article
  14. Hypertension: the missing WNKs.American journal of physiology. Renal physiology · 2016
    Review
  15. Maintaining KAmerican journal of physiology. Renal physiology · 2016
    Review
  16. Potassium and Its Discontents: New Insight, New Treatments.Journal of the American Society of Nephrology : JASN · 2016
    Review
  17. Review
  18. Article
  19. GermlineCancer genomics & proteomics
    Article
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.

Chou-Long HuangDepartment of Internal Medicine, Division of Nephrology, UT Southwestern Medical Center, 5323 Harry Hines Blvd., Dallas, TX, 75390-8856, USA. Chou-Long.Huang@UTSouthwestern.edu.
Chih-Jen ChengDepartment of Medicine, Division of Nephrology, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan.

Funding

Membrane Trafficking of Renal Potassium ChannelR01DK059530 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI HUANG, CHOU-LONG · 2003 to 2014
$4.7M
NIDDK NIH HHS DK59530NIDDK NIH HHS R01 DK059530
6 · The paper itself

Abstract

Mammalian with-no-lysine [K] (WNK) kinases are a family of four serine-threonine protein kinases, WNK1-4. Mutations of WNK1 and WNK4 in humans cause pseudohypoaldosteronism type II (PHA2), an autosomal-dominant disease characterized by hypertension and hyperkalemia. Increased Na(+) reabsorption through Na(+)-Cl(-) cotransporter (NCC) in the distal convoluted tubule plays an important role in the pathogenesis of hypertension in patients with PHA2. However, how WNK1 and WNK4 regulate NCC and how mutations of WNKs cause activation of NCC have been controversial. Here, we review current state of literature supporting a compelling model that WNK1 and WNK4 both contribute to stimulation of NCC. The precise combined effects of WNK1 and WNK4 on NCC remain unclear but likely are positive rather than antagonistic. The recent discovery that WNK kinases may function as an intracellular chloride sensor adds a new dimension to the physiological role of WNK kinases. Intracellular chloride-dependent regulation of WNK's may underlie the mechanism of regulation of NCC by extracellular K(+). Definite answer yet will require future investigation by tubular perfusion in mice with altered WNK kinase expression.

Indexed as

AnimalsHumansProtein KinasesSodium Chloride SymportersProtein KinasesSodium Chloride SymportersCullin3Kelch-likeNCCNKCC2WNK1WNK4

Identifiers

PMID25904388
PMCPMC4601926

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.