Evidence map›Paper›PMID 20231442›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2010

Mouse cystic fibrosis transmembrane conductance regulator forms cAMP-PKA-regulated apical chloride channels in cortical collecting duct.

Ming Lu, Ke Dong, Marie E Egan, Gerhard H Giebisch, Emile L Boulpaep, Steven C Hebert

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

13 citing papers in PubMed, 31 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Coordinated Control of ENaC and Na+,K+-ATPase in Renal Collecting Duct.Journal of the American Society of Nephrology : JASN · 2016
    Review
  5. The multiple roles of pendrin in the kidney.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2015
    Review
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Review
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

6 authors at 1 institution in 1 country.

Ming LuDepartment of Cellular and Molecular Physiology, Yale University School of Medicine, New Haven, CT 06520-8026, USA.
Ke Dong
Marie E Egan
Gerhard H Giebisch
Emile L Boulpaep
Steven C Hebert
Yale University · US

Funding

The Regulation of Renal Epithelial Cell Junction Assembly and PolarizationP01DK017433 · NIDDK · YALE UNIVERSITY · PI FORBUSH, BLISS · 1986 to 2018
$29.5M
CFTR REGULATION OF ION CHANNELSR01DK053428 · NIDDK · YALE UNIVERSITY · PI EGAN, MARIE E · 1998 to 2006
$1.4M
NIDDK NIH HHS P01 DK017433NIDDK NIH HHS P01 DK17433NIDDK NIH HHS R01 DK053428
6 · The paper itself

Abstract

The cystic fibrosis transmembrane conductance regulator (CFTR) is expressed in many segments of the mammalian nephron, where it may interact with and modulate the activity of a variety of apical membrane proteins, including the renal outer medullary potassium (ROMK) K(+) channel. However, the expression of CFTR in apical cell membranes or its function as a Cl(-) channel in native renal epithelia has not been demonstrated. Here, we establish that CFTR forms protein kinase A (PKA)-activated Cl(-) channels in the apical membrane of principal cells from the cortical collecting duct obtained from mice. These Cl(-) channels were observed in cell-attached apical patches of principal cells after stimulation by forskolin/3-isobutyl-1-methylxanthine. Quiescent Cl(-) channels were present in patches excised from untreated tubules because they could be activated after exposure to Mg-ATP and the catalytic subunit of PKA. The single-channel conductance, kinetics, and anion selectivity of these Cl(-) channels were the same as those of recombinant mouse CFTR channels expressed in Xenopus laevis oocytes. The CFTR-specific closed-channel blocker CFTR(inh)-172 abolished apical Cl(-) channel activity in excised patches. Moreover, apical Cl(-) channel activity was completely absent in principal cells from transgenic mice expressing the DeltaF508 CFTR mutation but was present and unaltered in ROMK-null mice. We discuss the physiologic implications of open CFTR Cl(-) channels on salt handling by the collecting duct and on the functional CFTR-ROMK interactions in modulating the metabolic ATP-sensing of ROMK.

Indexed as

AnimalsBenzoatesChloride ChannelsCyclic AMPCyclic AMP-Dependent Protein KinasesCystic Fibrosis Transmembrane Conductance RegulatorFemaleIn Vitro TechniquesKidney CortexKidney Tubules, CollectingKineticsMiceMice, Inbred C57BLMice, Inbred CFTRMice, KnockoutMice, Transgenic3-((3-trifluoromethyl)phenyl)-5-((3-carboxyphenyl)methylene)-2-thioxo-4-thiazolidinoneBenzoatesChloride ChannelsCyclic AMPCyclic AMP-Dependent Protein KinasesCystic Fibrosis Transmembrane Conductance RegulatorKcnj1 protein, mousePotassium Channels, Inwardly RectifyingRecombinant ProteinsThiazolidines

Identifiers

PMID20231442
PMCPMC2851921
OpenAlexW1968193812

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.