Evidence map›Paper›PMID 27474090›Full record

ReviewAmerican journal of physiology. Lung cellular and molecular physiology2016

Trafficking and function of the cystic fibrosis transmembrane conductance regulator: a complex network of posttranslational modifications.

Michelle L McClure, Stephen Barnes, Jeffrey L Brodsky, Eric J Sorscher

Abstract readReview
In one paragraph

Review in American journal of physiology. Lung cellular and molecular physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
–field-weighted citation impact
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

30 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Review
  5. CFTR as a therapeutic target for severe lung infection.American journal of physiology. Lung cellular and molecular physiology · 2025
    Review
  6. Article
  7. Article
  8. Intracellular Chloride Channels: A Rising Target in Lung Disease Research.Journal of respiratory biology and translational medicine · 2025
    Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. KDM2A and KDM3B as Potential Targets for the Rescue of F508del-CFTR.International journal of molecular sciences · 2022
    Article
  14. Palmitoylation of Voltage-Gated Ion Channels.International journal of molecular sciences · 2022
    Review
  15. TMED3 Complex Mediates ER Stress-Associated Secretion of CFTR, Pendrin, and SARS-CoV-2 Spike.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022
    Article
  16. Review
  17. Revisiting CFTR Interactions: Old Partners and New Players.International journal of molecular sciences · 2021
    Review
  18. Article
  19. Article
  20. 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

4 authors.

Michelle L McClureCystic Fibrosis Research Center, University of Alabama at Birmingham, Birmingham, Alabama.
Stephen BarnesDepartment of Pharmacology and Toxicology, University of Alabama at Birmingham, Birmingham, Alabama.
Jeffrey L BrodskyDepartment of Biological Sciences, University of Pittsburgh, Pittsburgh, Pennsylvania; and.
Eric J SorscherDepartment of Pediatrics, Emory University, Atlanta, Georgia esorscher@emory.edu.

Funding

Single Nephron and MetabolomicsP30DK079307 · NIDDK · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI KLEYMAN, THOMAS R · 2008 to 2022
$13.4M
ER Associated Degradation of Membrane Proteins in YeastR01GM075061 · NIGMS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI BRODSKY, JEFFREY L. · 2006 to 2019
$3.2M
NIDDK NIH HHS P30 DK079307NIGMS NIH HHS R01 GM075061
6 · The paper itself

Abstract

Posttranslational modifications add diversity to protein function. Throughout its life cycle, the cystic fibrosis transmembrane conductance regulator (CFTR) undergoes numerous covalent posttranslational modifications (PTMs), including glycosylation, ubiquitination, sumoylation, phosphorylation, and palmitoylation. These modifications regulate key steps during protein biogenesis, such as protein folding, trafficking, stability, function, and association with protein partners and therefore may serve as targets for therapeutic manipulation. More generally, an improved understanding of molecular mechanisms that underlie CFTR PTMs may suggest novel treatment strategies for CF and perhaps other protein conformational diseases. This review provides a comprehensive summary of co- and posttranslational CFTR modifications and their significance with regard to protein biogenesis.

Indexed as

Protein Processing, Post-TranslationalAnimalsCystic FibrosisCystic Fibrosis Transmembrane Conductance RegulatorGlycosylationHumansPhosphorylationProtein StabilityProtein TransportCFTR protein, humanCystic Fibrosis Transmembrane Conductance Regulatorcystic fibrosisglycosylationpalmitoylationphosphorylationprotein traffickingubiquitination

Identifiers

PMID27474090
PMCPMC5142128

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.