Evidence map›Paper›PMID 21248166›Full record

ReviewPhysiological reviews2011

The WNKs: atypical protein kinases with pleiotropic actions.

James A McCormick, David H Ellison

Open access · greenAbstract readReview
In one paragraph

Review in Physiological reviews, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 153 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
153citing papers in PubMed, 2 pooled it
11.8field-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

153 citing papers in PubMed, 2 syntheses or guidelines pooled it, 271 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Review
  4. Article
  5. Article
  6. Article
  7. Central Osmolality Sensing for Arginine Vasopressin Release Is Mediated by WNK1-OSR1/SPAK-Kv3.1 Cascade.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. The evolving concepts of KS-WNK1 effect on NCC activity.American journal of physiology. Renal physiology · 2025
    Review
  13. Review
  14. Familial Hyperkalemic Hypertension.Comprehensive Physiology · 2024
    Review
  15. Article
  16. Review
  17. Article
  18. Deletion of KS-WNK1 promotes NCC activation by increasing WNK1/4 abundance.American journal of physiology. Renal physiology · 2024
    Article
  19. Review
  20. Article

93 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 1 institution in 1 country.

James A McCormickDivision of Nephrology and Hypertension, Oregon Health and Science University and Veterans Affairs Medical Center, Portland, Oregon 97239, USA. mccormij@ohsu.edu
David H Ellison
Oregon Health & Science University · US

Funding

WNK Kinase Regulation of Thiazide-sensitive NaCl TransportR01DK051496 · NIDDK · UNIVERSITY OF COLORADO DENVER · PI David Hoadley Ellison, CHAO-LING YANG · 1998 to 2026
$8.4M
Analysis of distal conboluted tubule function in vivoK01DK076617 · NIDDK · OREGON HEALTH & SCIENCE UNIVERSITY · PI MCCORMICK, JAMES A · 2008 to 2012
$708k
NIDDK NIH HHS DK-51496NIDDK NIH HHS K01 DK076617NIDDK NIH HHS K01-DK-076617NIDDK NIH HHS R01 DK051496
6 · The paper itself

Abstract

WNKs are serine/threonine kinases that comprise a unique branch of the kinome. They are so-named owing to the unusual placement of an essential catalytic lysine. WNKs have now been identified in diverse organisms. In humans and other mammals, four genes encode WNKs. WNKs are widely expressed at the message level, although data on protein expression is more limited. Soon after the WNKs were identified, mutations in genes encoding WNK1 and -4 were determined to cause the human disease familial hyperkalemic hypertension (also known as pseudohypoaldosteronism II, or Gordon's Syndrome). For this reason, a major focus of investigation has been to dissect the role of WNK kinases in renal regulation of ion transport. More recently, a different mutation in WNK1 was identified as the cause of hereditary sensory and autonomic neuropathy type II, an early-onset autosomal disease of peripheral sensory nerves. Thus the WNKs represent an important family of potential targets for the treatment of human disease, and further elucidation of their physiological actions outside of the kidney and brain is necessary. In this review, we describe the gene structure and mechanisms regulating expression and activity of the WNKs. Subsequently, we outline substrates and targets of WNKs as well as effects of WNKs on cellular physiology, both in the kidney and elsewhere. Next, consequences of these effects on integrated physiological function are outlined. Finally, we discuss the known and putative pathophysiological relevance of the WNKs.

Indexed as

Amino Acid SequenceAnimalsBase SequenceDrug Delivery SystemsGene Expression RegulationGenetic PleiotropyHereditary Sensory and Autonomic NeuropathiesHumansHypertensionIntracellular Signaling Peptides and ProteinsMinor Histocompatibility AntigensMolecular Sequence DataMultigene FamilyNeoplasmsProtein Serine-Threonine KinasesPseudohypoaldosteronismIntracellular Signaling Peptides and ProteinsMinor Histocompatibility AntigensProtein Serine-Threonine KinasesWNK1 protein, humanWNK Lysine-Deficient Protein Kinase 1

Identifiers

PMID21248166
PMCPMC3035565
OpenAlexW2172151601

What OpenQuestion holds

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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.