Evidence map›Paper›PMID 23195681›Full record

ArticleAmerican journal of physiology. Renal physiology2013

Kidney-specific WNK1 regulates sodium reabsorption and potassium secretion in mouse cortical collecting duct.

Chih-Jen Cheng, Michel Baum, Chou-Long Huang

Abstract read
In one paragraph

Article in American journal of physiology. Renal physiology, 2013. 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
1.1field-weighted citation impact, top 24% 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

19 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. Article
  3. The evolving concepts of KS-WNK1 effect on NCC activity.American journal of physiology. Renal physiology · 2025
    Review
  4. Deletion of KS-WNK1 promotes NCC activation by increasing WNK1/4 abundance.American journal of physiology. Renal physiology · 2024
    Article
  5. Review
  6. Article
  7. Review
  8. NCC regulation by WNK signal cascade.Frontiers in physiology · 2022
    Review
  9. Review
  10. Role of WNK4 and kidney-specific WNK1 in mediating the effect of high dietary KAmerican journal of physiology. Renal physiology · 2018
    Article
  11. Article
  12. New options for the management of chronic hyperkalemia.Kidney international supplements · 2017
    Review
  13. Hypertension: the missing WNKs.American journal of physiology. Renal physiology · 2016
    Review
  14. Review
  15. Article
  16. Dietary potassium and the renal control of salt balance and blood pressure.Pflugers Archiv : European journal of physiology · 2015
    Review
  17. Distal convoluted tubule.Clinical journal of the American Society of Nephrology : CJASN · 2014
    Review
  18. Article
  19. 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

3 authors at 3 institutions in 2 countries.

Chih-Jen ChengDepartment of Medicine, Division of Nephrology, UT Southwestern Medical Center, Dallas, TX 75390, USA.
Michel Baum
Chou-Long Huang
Southwestern Medical CenterSouthwestern Medical Center · USThe University of Texas Southwestern Medical Center · US

Funding

UT Southwestern O'Brien Kidney Research Core CenterP30DK079328 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI MOE, ORSON W · 2007 to 2021
$16.9M
Membrane Trafficking of Renal Potassium ChannelR01DK059530 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI HUANG, CHOU-LONG · 2003 to 2014
$4.7M
Neonatal Proximal Tubule AcidificationR01DK041612 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI BAUM, MICHEL GERARD, MOE, ORSON W · 1991 to 2013
$2.7M
NIDDK NIH HHS DK41612NIDDK NIH HHS DK59530NIDDK NIH HHS DK79328NIDDK NIH HHS R01 DK059530
6 · The paper itself

Abstract

Kidney-specific with-no-lysine kinase 1 (KS-WNK1) is a kinase-deficient variant of WNK1 that is expressed exclusively in the kidney. It is abundantly expressed in the distal convoluted tubule (DCT) and to a lesser extent in the cortical thick ascending limb (cTAL), connecting tubule, and cortical collecting duct (CCD). KS-WNK1 inhibits Na(+)-K(+)-2Cl(-)- and sodium chloride cotransporter-mediated Na(+) reabsorption in cTAL and DCT, respectively. Here, we investigated the role of KS-WNK1 in regulating Na(+) and K(+) transport in CCD using in vitro microperfusion of tubules isolated from KS-WNK1 knockout mice and control wild-type littermates. Because baseline K(+) secretion and Na(+) reabsorption were negligible in mouse CCD, we studied tubules isolated from mice fed a high-K(+) diet for 2 wk. Compared with that in wild-type tubules, K(+) secretion was reduced in KS-WNK1 knockout CCD perfused at a low luminal fluid rate of ~1.5 nl/min. Na(+) reabsorption and the lumen-negative transepithelial potential difference were also lower in the KS-WNK1 knockout CCD compared with control CCD. Increasing the perfusion rate to ~5.5 nl/min stimulated K(+) secretion in the wild-type as well as knockout CCD. The magnitudes of flow-stimulated increase in K(+) secretion were similar in wild-type and knockout CCD. Maxi-K(+) channel inhibitor iberiotoxin had no effect on K(+) secretion when tubules were perfused at ~1.5 nl/min, but completely abrogated the flow-dependent increase in K(+) secretion at ~5.5 nl/min. These findings support the notion that KS-WNK1 stimulates ROMK-mediated K(+) secretion, but not flow-dependent K(+) secretion mediated by maxi-K(+) channels in CCD. In addition, KS-WNK1 plays a role in regulating Na(+) transport in the CCD.

Indexed as

AbsorptionAnimalsExonsFemaleKidney Tubules, CollectingKidney Tubules, DistalLarge-Conductance Calcium-Activated Potassium ChannelsMaleMembrane PotentialsMiceMice, KnockoutMinor Histocompatibility AntigensPeptidesPerfusionPotassiumPotassium Channels, Inwardly RectifyingiberiotoxinKcnj1 protein, mouseLarge-Conductance Calcium-Activated Potassium ChannelsMinor Histocompatibility AntigensPeptidesPotassiumPotassium Channels, Inwardly RectifyingPotassium, DietaryProtein Serine-Threonine KinasesSodiumWnk1 protein, mouseWNK Lysine-Deficient Protein Kinase 1

Identifiers

PMID23195681
PMCPMC3566501
OpenAlexW2092742344

What OpenQuestion holds

Textmetadata
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.