Evidence map›Paper›PMID 17084917›Full record

ArticleBiochimica et biophysica acta2007

CFTR surface expression and chloride currents are decreased by inhibitors of N-WASP and actin polymerization.

Radhika Ganeshan, Krzysztof Nowotarski, Anke Di, Deborah J Nelson, Kevin L Kirk

Abstract read
In one paragraph

Article in Biochimica et biophysica acta, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.2field-weighted citation impact, top 23% 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

14 citing papers in PubMed, 38 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. CK19 stabilizes CFTR at the cell surface by limiting its endocytic pathway degradation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019
    Article
  5. Article
  6. Article
  7. Regulators of Actin Dynamics in Gastrointestinal Tract Tumors.Gastroenterology research and practice · 2015
    Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. 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

5 authors at 2 institutions in 1 country.

Radhika GaneshanDepartment of Physiology and Biophysics, Gregory Fleming James Cystic Fibrosis Research Center, University of Alabama at Birmingham, 1918 University Blvd., MCLM 985, Birmingham, AL 35294, USA.
Krzysztof Nowotarski
Anke Di
Deborah J Nelson
Kevin L Kirk
University of Alabama at Birmingham · USUniversity of Chicago · US

Funding

REGULATION OF CFTR BY SYNTAXIN AND N-SEC 1 ISOFORMSR01HL058341 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI KIRK, KEVIN L · 1996 to 2011
$2.8M
NHLBI NIH HHS HL 58341NHLBI NIH HHS R01 HL058341
6 · The paper itself

Abstract

The cystic fibrosis transmembrane conductance regulator (CFTR) undergoes rapid turnover at the plasma membrane in various cell types. The ubiquitously expressed N-WASP promotes actin polymerization and regulates endocytic trafficking of other proteins in response to signaling molecules such as Rho-GTPases. In the present study we investigated the effects of wiskostatin, an N-WASP inhibitor, on the surface expression and activity of CFTR. We demonstrate, using surface biotinylation methods, that the steady-state surface CFTR pool in stably transfected BHK cells was dramatically decreased following wiskostatin treatment with a corresponding increase in the amount of intracellular CFTR. Similar effects were observed for latrunculin B, a specific actin-disrupting reagent. Both reagents strongly inhibited macroscopic CFTR-mediated Cl(-) currents in two cell types including HT29-Cl19A colonic epithelial cells. As previously reported, CFTR internalization from the cell surface was strongly inhibited by a cyclic-AMP cocktail. This effect of cyclic-AMP was only partially blunted in the presence of wiskostatin, which raises the possibility that these two factors modulate different steps in CFTR traffic. In kinetic studies wiskostatin appeared to accelerate the initial rate of CFTR endocytosis as well as inhibit its recycling back to the cell surface over longer time periods. Our studies implicate a role for N-WASP-mediated actin polymerization in regulating CFTR surface expression and channel activity.

Indexed as

ActinsAnimalsBiotinylationBridged Bicyclo Compounds, HeterocyclicCarbazolesCell MembraneColonCricetinaeCyclic AMPCystic Fibrosis Transmembrane Conductance RegulatorDose-Response Relationship, DrugEndocytosisEpithelial CellsHT29 CellsHumansIon Channel GatingActinsBridged Bicyclo Compounds, HeterocyclicCarbazolesCyclic AMPCystic Fibrosis Transmembrane Conductance Regulatorlatrunculin BPropanolaminesThiazolidineswiskostatinWiskott-Aldrich Syndrome Protein, Neuronal

Identifiers

PMID17084917
PMCPMC1828603
OpenAlexW2096770575

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.