Evidence map›Paper›PMID 22718890›Full record

ArticleAmerican journal of physiology. Renal physiology2012

A new model of the distal convoluted tubule.

Benjamin Ko, Abinash C Mistry, Lauren Hanson, Rickta Mallick, Leslie L Cooke, Bradley K Hack, Patrick Cunningham, Robert S Hoover

Open access · hybridAbstract read
In one paragraph

Article in American journal of physiology. Renal physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

31 citing papers in PubMed, 47 citations in OpenAlex.

  1. Article
  2. Article
  3. PIPBiology · 2022
    Article
  4. Article
  5. Article
  6. Article
  7. Deletion of Kir5.1 abolishes the effect of high NaAmerican journal of physiology. Renal physiology · 2021
    Article
  8. Zinc deficiency induces hypertension by promoting renal NaAmerican journal of physiology. Renal physiology · 2019
    Article
  9. Article
  10. Potassium conservation is impaired in mice with reduced renal expression of Kir4.1.American journal of physiology. Renal physiology · 2018
    Article
  11. Article
  12. Article
  13. Article
  14. CD8Nature communications · 2017
    Article
  15. Article
  16. Article
  17. Article
  18. PTH modulation of NCC activity regulates TRPV5 Ca2+ reabsorption.American journal of physiology. Renal physiology · 2016
    Article
  19. Article
  20. The Effect of WNK4 on the Na+-Cl- Cotransporter Is Modulated by Intracellular Chloride.Journal of the American Society of Nephrology : JASN · 2015
    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

8 authors at 2 institutions in 1 country.

Benjamin KoDepartment of Medicine, University of Chicago, Chicago, Illinois, USA.
Abinash C Mistry
Lauren Hanson
Rickta Mallick
Leslie L Cooke
Bradley K Hack
Patrick Cunningham
Robert S Hoover
University of Chicago · USEmory University · US

Funding

Endothelial Injury in Endotoxin-Induced Acute Renal FailureR01DK080863 · NIDDK · UNIVERSITY OF CHICAGO · PI CUNNINGHAM, PATRICK N · 2010 to 2014
$1.7M
Mechanisms of Hormonal Regulation of the Sodium Chloride CotransporterR01DK085097 · NIDDK · EMORY UNIVERSITY · PI HOOVER, ROBERT S · 2010 to 2015
$1.5M
The Role of Ubiquitin in Sodium Chloride Co-Transporter RegulationK08DK081728 · NIDDK · UNIVERSITY OF CHICAGO · PI KO, BENJAMIN S · 2008 to 2012
$691k
NIDDK NIH HHS K08-DK 081728NIDDK NIH HHS R01-DK-080863NIDDK NIH HHS R01 DK085097NIDDK NIH HHS R01-DK-085097
6 · The paper itself

Abstract

The Na(+)-Cl(-) cotransporter (NCC) in the distal convoluted tubule (DCT) of the kidney is a key determinant of Na(+) balance. Disturbances in NCC function are characterized by disordered volume and blood pressure regulation. However, many details concerning the mechanisms of NCC regulation remain controversial or undefined. This is partially due to the lack of a mammalian cell model of the DCT that is amenable to functional assessment of NCC activity. Previously reported investigations of NCC regulation in mammalian cells have either not attempted measurements of NCC function or have required perturbation of the critical without a lysine kinase (WNK)/STE20/SPS-1-related proline/alanine-rich kinase regulatory pathway before functional assessment. Here, we present a new mammalian model of the DCT, the mouse DCT15 (mDCT15) cell line. These cells display native NCC function as measured by thiazide-sensitive, Cl(-)-dependent (22)Na(+) uptake and allow for the separate assessment of NCC surface expression and activity. Knockdown by short interfering RNA confirmed that this function was dependent on NCC protein. Similar to the mammalian DCT, these cells express many of the known regulators of NCC and display significant baseline activity and dimerization of NCC. As described in previous models, NCC activity is inhibited by appropriate concentrations of thiazides, and phorbol esters strongly suppress function. Importantly, they display release of WNK4 inhibition of NCC by small hairpin RNA knockdown. We feel that this new model represents a critical tool for the study of NCC physiology. The work that can be accomplished in such a system represents a significant step forward toward unraveling the complex regulation of NCC.

Indexed as

AnimalsCell LineHippo KinasesKidney Tubules, DistalMiceModels, AnimalProtein Serine-Threonine KinasesSodium Chloride SymportersThiazidesHippo KinasesPAS domain kinasesPrkwnk4 protein, mouseProtein Serine-Threonine KinasesSLK protein, mouseSodium Chloride SymportersThiazides

Identifiers

PMID22718890
PMCPMC3468492
OpenAlexW2106365130

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.