Evidence map›Paper›PMID 30893953›Full record

ReviewGenes2019

Cell-Selective Regulation of CFTR Gene Expression: Relevance to Gene Editing Therapeutics.

Hannah Swahn, Ann Harris

Abstract readReview
In one paragraph

Review in Genes, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing 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

21 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. CFTR and Gastrointestinal Cancers: An Update.Journal of personalized medicine · 2022
    Review
  8. Article
  9. Revisiting CFTR Interactions: Old Partners and New Players.International journal of molecular sciences · 2021
    Review
  10. Review
  11. Article
  12. OTX2 regulates CFTR expression during endoderm differentiation and occupies 3' cis-regulatory elements.Developmental dynamics : an official publication of the American Association of Anatomists · 2021
    Article
  13. International journal of molecular sciences · 2021
    Article
  14. Article
  15. Article
  16. Cystic Fibrosis, CFTR, and Colorectal Cancer.International journal of molecular sciences · 2020
    Review
  17. Article
  18. Optical Nanosensors forAnalytical methods : advancing methods and applications · 2020
    Article
  19. Genetic variation in CFTR and modifier loci may modulate cystic fibrosis disease severity.Journal of cystic fibrosis : official journal of the European Cystic Fibrosis Society · 2020
    Review
  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

2 authors.

Hannah SwahnDepartment of Genetics and Genome Sciences, Case Western Reserve University, Cleveland, OH 44067, USA. hls68@case.edu.
Ann HarrisDepartment of Genetics and Genome Sciences, Case Western Reserve University, Cleveland, OH 44067, USA. ann.harris@case.edu.

Funding

GRADUATE TRAINING IN CELLULAR AND MOLECULAR BIOLOGYT32GM008056 · NIGMS · CASE WESTERN RESERVE UNIVERSITY · PI DIEHL, JOHN ALAN, SNIDER, MARTIN D · 1985 to 2019
$7.1M
NIGMS NIH HHS T32 GM008056NIH HHS HL094585
6 · The paper itself

Abstract

The cystic fibrosis transmembrane conductance regulator (CFTR) gene is an attractive target for gene editing approaches, which may yield novel therapeutic approaches for genetic diseases such as cystic fibrosis (CF). However, for gene editing to be effective, aspects of the three-dimensional (3D) structure and cis-regulatory elements governing the dynamic expression of CFTR need to be considered. In this review, we focus on the higher order chromatin organization required for normal CFTR locus function, together with the complex mechanisms controlling expression of the gene in different cell types impaired by CF pathology. Across all cells, the CFTR locus is organized into an invariant topologically associated domain (TAD) established by the architectural proteins CCCTC-binding factor (CTCF) and cohesin complex. Additional insulator elements within the TAD also recruit these factors. Although the CFTR promoter is required for basal levels of expression, cis-regulatory elements (CREs) in intergenic and intronic regions are crucial for cell-specific and temporal coordination of CFTR transcription. These CREs are recruited to the promoter through chromatin looping mechanisms and enhance cell-type-specific expression. These features of the CFTR locus should be considered when designing gene-editing approaches, since failure to recognize their importance may disrupt gene expression and reduce the efficacy of therapies.

Indexed as

CCCTC-Binding FactorCell Cycle ProteinsChromatinChromosomal Proteins, Non-HistoneCohesinsCystic Fibrosis Transmembrane Conductance RegulatorGene EditingGene Expression RegulationGenetic LociHumansOrgan SpecificityPromoter Regions, GeneticProtein DomainsCCCTC-Binding FactorCell Cycle ProteinsCFTR protein, humanChromatinChromosomal Proteins, Non-HistoneCohesinsCTCF protein, humanCystic Fibrosis Transmembrane Conductance RegulatorCFTRchromatin architecturecis-regulatory elementsCRISPR/Cas9enhancersgene editingtranscription factors

Identifiers

PMID30893953
PMCPMC6471542

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.