Evidence map›Paper›PMID 24313290›Full record

ReviewBiology of the cell2014

Regulation of with-no-lysine kinase signaling by Kelch-like proteins.

Shinichi Uchida, Eisei Sohara, Tatemitsu Rai, Sei Sasaki

Open access · hybridAbstract readReview
In one paragraph

Review in Biology of the cell, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

17 citing papers in PubMed, 34 citations in OpenAlex.

  1. Genome-wide identification and expression analysis of the WNK kinase gene family in soybean.Molecular breeding : new strategies in plant improvement · 2024
    Article
  2. Genome-Wide Identification and Expression Analysis ofInternational journal of molecular sciences · 2023
    Article
  3. Review
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  10. Molecular and cellular biology · 2017
    Article
  11. A patient with pseudohypoaldosteronism type II complicated by congenital hypopituitarism carrying aClinical pediatric endocrinology : case reports and clinical investigations : official journal of the Japanese Society for Pediatric Endocrinology · 2016
    Article
  12. Hypertension: the missing WNKs.American journal of physiology. Renal physiology · 2016
    Review
  13. Article
  14. Gordon Syndrome: a continuing story.Pediatric nephrology (Berlin, Germany) · 2015
    Review
  15. Article
  16. Article
  17. 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

4 authors at 1 institution in 1 country.

Shinichi UchidaDepartment of Nephrology, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, 1-5-45 Yushima, Bunkyo-ku, Tokyo, 113-8519, Japan.
Eisei Sohara
Tatemitsu Rai
Sei Sasaki
Tokyo Medical and Dental University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In 2001, with-no-lysine (WNK) kinases were identified as the genes responsible for the human hereditary hypertensive disease pseudohypoaldosteronism type II (PHAII). It took a further 6 years to clarify that WNK kinases participate in a signaling cascade with oxidative stress-responsive gene 1 (OSR1), Ste20-related proline-alanine-rich kinase (SPAK), and thiazide-sensitive NaCl cotransporter (NCC) in the kidney and the constitutive activation of this signaling cascade is the molecular basis of PHAII. Since this discovery, the WNK-OSR1/SPAK-NCC signaling cascade has been shown to be involved not only in PHAII but also in the regulation of blood pressure under normal and pathogenic conditions, such as hyperinsulinemia. However, the molecular mechanisms of WNK kinase regulation by dietary and hormonal factors and by PHAII-causing mutations remain poorly understood. In 2012, two additional genes responsible for PHAII, Kelch-like 3 (KLHL3) and Cullin3, were identified. At the time of their discovery, the molecular mechanisms underlying the interaction between these genes and their involvement in PHAII were unknown. Here we review the pathophysiological roles of the WNK signaling cascade clarified to date and introduce a new mechanism of WNK kinase regulation by KLHL3 and Cullin3, which provides insight on previously unknown mechanisms of WNK kinase regulation.

Indexed as

Signal TransductionAdaptor Proteins, Signal TransducingAnimalsCarrier ProteinsCullin ProteinsHumansIntracellular Signaling Peptides and ProteinsMicrofilament ProteinsMinor Histocompatibility AntigensProtein Serine-Threonine KinasesPseudohypoaldosteronismWNK Lysine-Deficient Protein Kinase 1Adaptor Proteins, Signal TransducingCarrier ProteinsCUL3 protein, humanCullin ProteinsIntracellular Signaling Peptides and ProteinsKLHL3 protein, humanMicrofilament ProteinsMinor Histocompatibility AntigensProtein Serine-Threonine KinasesSTK39 protein, humanWNK1 protein, humanWNK Lysine-Deficient Protein Kinase 1HypertensionKidneyKinasesMembrane transportUbiquitin

Identifiers

PMID24313290
PMCPMC4162998
OpenAlexW1786333316

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.