Evidence map›Paper›PMID 18285607›Full record

ArticleMolecular & cellular proteomics : MCP2008

Chemical rescue of deltaF508-CFTR mimics genetic repair in cystic fibrosis bronchial epithelial cells.

Om V Singh, Harvey B Pollard, Pamela L Zeitlin

Open access · hybridAbstract read
In one paragraph

Article in Molecular & cellular proteomics : MCP, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
3.7field-weighted citation impact, top 7% 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

36 citing papers in PubMed, 65 citations in OpenAlex.

  1. Review
  2. Article
  3. Novel PTH Gene Mutations Causing Isolated Hypoparathyroidism.The Journal of clinical endocrinology and metabolism · 2022
    Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Syntaxin 8 and the Endoplasmic Reticulum Processing of ΔF508-CFTR.Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · 2018
    Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Junctional abnormalities in human airway epithelial cells expressing F508del CFTR.American journal of physiology. Lung cellular and molecular physiology · 2015
    Article
  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

3 authors at 2 institutions in 1 country.

Om V SinghDepartment of Pediatrics, The Johns Hopkins School of Medicine, Baltimore, Maryland 21287, USA.
Harvey B Pollard
Pamela L Zeitlin
Johns Hopkins University · USUniformed Services University of the Health Sciences · US

Funding

CHLORIDE CHANNELS IN LUNG DEVELOPMENTR01HL059410 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI ZEITLIN, PAMELA L. · 2000 to 2012
$3.8M
NHLBI NIH HHS N01 BAA HL 02-04NHLBI NIH HHS R01 HL059410NHLBI NIH HHS R01 HL 59410
6 · The paper itself

Abstract

In a previous study of sodium 4-phenylbutyrate (4-PBA)-responsive proteins in cystic fibrosis (CF) IB3-1 bronchial epithelial cells, we identified 85 differentially expressed high abundance proteins from whole cellular lysate (Singh, O. V., Vij, N., Mogayzel, P. J., Jr., Jozwik, C., Pollard, H. B., and Zeitlin, P. L. (2006) Pharmacoproteomics of 4-phenylbutyrate-treated IB3-1 cystic fibrosis bronchial epithelial cells. J. Proteome Res. 5, 562-571). In the present work we hypothesize that a subset of heat shock proteins that interact with cystic fibrosis transmembrane conductance regulator (CFTR) in common during chemical rescue and genetic repair will identify therapeutic networks for targeted intervention. Immunocomplexes were generated from total cellular lysates, and three subcellular fractions (endoplasmic reticulum (ER), cytosol, and plasma membrane) with anti-CFTR polyclonal antibody from CF (IB3-1), chemically rescued CF (4-PBA-treated IB3-1), and genetically repaired CF (IB3-1/S9 daughter cells repaired by gene transfer with adeno-associated virus-(wild type) CFTR). CFTR-interacting proteins were analyzed on two-dimensional gels and identified by mass spectrometry. A set of 16 proteins known to act in ER-associated degradation were regulated in common and functionally connected to the protein processing, protein folding, and inflammatory response. Some of these proteins were modulated exclusively in ER, cytosol, or plasma membrane. A subset of 4-PBA-modulated ER-associated degradation chaperones (GRP94, HSP84, GRP78, GRP75, and GRP58) was observed to associate with the immature B form of CFTR in ER. HSP70 and HSC70 interacted with the C band (mature form) of CFTR at the cell surface. We conclude that chemically rescued CFTR associates with a specific set of HSP70 family proteins that mark therapeutic interactions and can be useful to correct both ion transport and inflammatory phenotypes in CF subjects.

Indexed as

Gene Expression RegulationMutationBiological TransportBronchiCell MembraneComputational BiologyCystic Fibrosis Transmembrane Conductance RegulatorCytosolEndoplasmic ReticulumEndoplasmic Reticulum Chaperone BiPEpithelial CellsGenetic TherapyHumansInflammationMolecular ChaperonesSubcellular FractionsCFTR protein, humanCystic Fibrosis Transmembrane Conductance RegulatorEndoplasmic Reticulum Chaperone BiPHSPA5 protein, humanMolecular Chaperones

Identifiers

PMID18285607
PMCPMC2424193
OpenAlexW2158235616

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.