Evidence map›Paper›PMID 10675364›Full record

ArticleThe Journal of clinical investigation2000

Syntaxin 1A is expressed in airway epithelial cells, where it modulates CFTR Cl(-) currents.

A P Naren, A Di, E Cormet-Boyaka, P N Boyaka, J R McGhee, W Zhou, K Akagawa, T Fujiwara, U Thome, J F Engelhardt and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

26 citing papers in PubMed, 70 citations in OpenAlex.

  1. Article
  2. Revisiting CFTR Interactions: Old Partners and New Players.International journal of molecular sciences · 2021
    Review
  3. Article
  4. AP2 α modulates cystic fibrosis transmembrane conductance regulator function in the human intestine.Journal of cystic fibrosis : official journal of the European Cystic Fibrosis Society · 2017
    Article
  5. Article
  6. Article
  7. Article
  8. Characterization of CFTR High Expresser cells in the intestine.American journal of physiology. Gastrointestinal and liver physiology · 2013
    Article
  9. Article
  10. Physiology of epithelial chloride and fluid secretion.Cold Spring Harbor perspectives in medicine · 2012
    Article
  11. Analysis of CFTR interactome in the macromolecular complexes.Methods in molecular biology (Clifton, N.J.) · 2011
    Article
  12. Article
  13. Article
  14. Article
  15. Regulation of the epithelial sodium channel by membrane trafficking.American journal of physiology. Renal physiology · 2009
    Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

12 authors at 4 institutions in 2 countries.

A P NarenGregory Fleming James Cystic Fibrosis Center and Department of Physiology and Biophysics, University of Alabama at Birmingham, Birmingham, Alabama 35294, USA.
A Di
E Cormet-Boyaka
P N Boyaka
J R McGhee
W Zhou
K Akagawa
T Fujiwara
U Thome
J F Engelhardt
D J Nelson
K L Kirk
University of Alabama at Birmingham · USKyorin University · JPUniversity of Chicago · USUniversity of Iowa · US

Funding

MODELS OF SUBMUCOSAL GLAND DEVELOPMENT AND FUNCTIONR01DK047967 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI ENGELHARDT, JOHN F · 1993 to 2020
$3.8M
RCFTR DEPENDENT MEMBRANE RECYCLING AND C1 TRANSPORTR01DK050830 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI KIRK, KEVIN L · 1995 to 1997
–
NIDDK NIH HHS DK 50830NIDDK NIH HHS DK 51868NIDDK NIH HHS R01 DK047967
6 · The paper itself

Abstract

The CFTR Cl(-) channel controls salt and water transport across epithelial tissues. Previously, we showed that CFTR-mediated Cl(-) currents in the Xenopus oocyte expression system are inhibited by syntaxin 1A, a component of the membrane trafficking machinery. This negative modulation of CFTR function can be reversed by soluble syntaxin 1A peptides and by the syntaxin 1A binding protein, Munc-18. In the present study, we determined whether syntaxin 1A is expressed in native epithelial tissues that normally express CFTR and whether it modulates CFTR currents in these tissues. Using immunoblotting and immunofluorescence, we observed syntaxin 1A in native gut and airway epithelial tissues and showed that epithelial cells from these tissues express syntaxin 1A at >10-fold molar excess over CFTR. Syntaxin 1A is seen near the apical cell surfaces of human bronchial airway epithelium. Reagents that disrupt the CFTR-syntaxin 1A interaction, including soluble syntaxin 1A cytosolic domain and recombinant Munc-18, augmented cAMP-dependent CFTR Cl(-) currents by more than 2- to 4-fold in mouse tracheal epithelial cells and cells derived from human nasal polyps, but these reagents did not affect CaMK II-activated Cl(-) currents in these cells.

Indexed as

AnimalsAntigens, SurfaceCells, CulturedChloride ChannelsCystic Fibrosis Transmembrane Conductance RegulatorEpithelial CellsHumansIon TransportMiceNerve Tissue ProteinsRespiratory SystemSyntaxin 1XenopusAntigens, SurfaceCFTR protein, humanChloride ChannelsCystic Fibrosis Transmembrane Conductance RegulatorNerve Tissue ProteinsSTX1A protein, humanStx1a protein, mouseSyntaxin 1

Identifiers

PMID10675364
PMCPMC377449
OpenAlexW2144590344

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.