Evidence map›Paper›PMID 1699127›Full record

ArticleNature1990

Expression and characterization of the cystic fibrosis transmembrane conductance regulator.

R J Gregory, S H Cheng, D P Rich, J Marshall, S Paul, K Hehir, L Ostedgaard, K W Klinger, M J Welsh, A E Smith

Abstract read
PubMed Publisher
In one paragraph

Article in Nature, 1990. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 107 papers.

0numbers the graph read from it
0cells of the map it votes in
107citing papers in PubMed
66.9field-weighted citation impact, top 1% 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

107 citing papers in PubMed, 344 citations in OpenAlex.

  1. Article
  2. Considerations for early life genetic therapies in cystic fibrosis.American journal of physiology. Lung cellular and molecular physiology · 2026
    Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  12. Review
  13. Rescue of CFTR NBD2 mutants N1303K and S1235R is influenced by the functioning of the autophagosome.Journal of cystic fibrosis : official journal of the European Cystic Fibrosis Society · 2018
    Article
  14. Cystic Fibrosis-Related Diabetes.Frontiers in endocrinology · 2018
    Review
  15. Article
  16. Article
  17. The CFTR trafficking mutation F508del inhibits the constitutive activity of SLC26A9.American journal of physiology. Lung cellular and molecular physiology · 2017
    Article
  18. Article
  19. Article
  20. Review

47 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 2 institutions in 1 country.

R J GregoryGenzyme Corporation, Framingham, Massachusetts.
S H Cheng
D P Rich
J Marshall
S Paul
K Hehir
L Ostedgaard
K W Klinger
M J Welsh
A E Smith
University of Iowa · USHoward Hughes Medical Institute · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cystic fibrosis (CF) is a common lethal genetic disease that manifests itself in airway and other epithelial cells as defective chloride ion absorption and secretion, resulting at least in part from a defect in a cyclic AMP-regulated, outwardly-rectifying Cl- channel in the apical surface. The gene responsible for CF has been identified and predicted to encode a membrane protein termed the CF transmembrane conductance regulator (CFTR). Identification of a cryptic bacterial promoter within the CFTR coding sequence led us to construct a complementary DNA in a low-copy-number plasmid, thereby avoiding the deleterious effects of CFTR expression on Escherischia coli. We have used this cDNA to express CFTR in vitro and in vivo. Here we demonstrate that CFTR is a membrane-associated glycoprotein that can be phosporylated in vitro by cAMP-dependent protein kinase. Polyclonal and monoclonal antibodies directed against distinct domains of the protein immunoprecipitated recombinant CFTR as well as the endogenous CFTR in nonrecombinant T84 cells. Partial proteolysis fingerprinting showed that the recombinant and non-recombinant proteins are indistinguishable. These data, which establish several characteristics of the protein responsible for CF, will now enable CFTR function to be studied and will provide a basis for diagnosis and therapy.

Indexed as

Gene ExpressionChloramphenicol O-AcetyltransferaseCyclic AMPCystic FibrosisCystic Fibrosis Transmembrane Conductance RegulatorDNAEscherichia coliHeLa CellsHumansMembrane ProteinsPhosphorylationPlasmidsPromoter Regions, GeneticProtein KinasesRecombinant ProteinsRestriction MappingCFTR protein, humanChloramphenicol O-AcetyltransferaseCyclic AMPCystic Fibrosis Transmembrane Conductance RegulatorDNAMembrane ProteinsProtein KinasesRecombinant Proteins

Identifiers

PMID1699127
OpenAlexW2036774130

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.