Evidence map›Paper›PMID 34404863›Full record

ArticleScientific reports2021

SFPQ rescues F508del-CFTR expression and function in cystic fibrosis bronchial epithelial cells.

Parameet Kumar, Dharmendra Kumar Soni, Chaitali Sen, Mads B Larsen, Krystyna Mazan-Mamczarz, Yulan Piao, Supriyo De, Myriam Gorospe, Raymond A Frizzell, Roopa Biswas

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.4field-weighted citation impact, top 35% 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

3 citing papers in PubMed, 3 citations in OpenAlex.

  1. Article
  2. CFTR and Gastrointestinal Cancers: An Update.Journal of personalized medicine · 2022
    Review
  3. 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

10 authors at 4 institutions in 1 country.

Parameet Kumar *Department of Anatomy, Physiology and Genetics, School of Medicine, Uniformed Services University of the Health Sciences, Bethesda, MD, 20814, USA.
Dharmendra Kumar Soni *Department of Anatomy, Physiology and Genetics, School of Medicine, Uniformed Services University of the Health Sciences, Bethesda, MD, 20814, USA.
Chaitali SenDepartment of Anatomy, Physiology and Genetics, School of Medicine, Uniformed Services University of the Health Sciences, Bethesda, MD, 20814, USA.
Mads B LarsenDepartment of Cell Biology, University of Pittsburgh, School of Medicine, Pittsburgh, PA, 1526, USA.
Krystyna Mazan-MamczarzLaboratory of Genetics and Genomics, National Institute on Aging, National Institutes of Health, Baltimore, MD, 21224-6825, USA.
Yulan PiaoLaboratory of Genetics and Genomics, National Institute on Aging, National Institutes of Health, Baltimore, MD, 21224-6825, USA.
Supriyo DeLaboratory of Genetics and Genomics, National Institute on Aging, National Institutes of Health, Baltimore, MD, 21224-6825, USA.
Myriam GorospeLaboratory of Genetics and Genomics, National Institute on Aging, National Institutes of Health, Baltimore, MD, 21224-6825, USA.
Raymond A FrizzellDepartment of Cell Biology, University of Pittsburgh, School of Medicine, Pittsburgh, PA, 1526, USA.
Roopa BiswasDepartment of Anatomy, Physiology and Genetics, School of Medicine, Uniformed Services University of the Health Sciences, Bethesda, MD, 20814, USA. roopa.biswas@usuhs.edu.
Uniformed Services University of the Health Sciences · USNational Institute on Aging · USUniversity of Pittsburgh · USNational Institutes of Health · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cystic fibrosis (CF) occurs as a result of mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene, which lead to misfolding, trafficking defects, and impaired function of the CFTR protein. Splicing factor proline/glutamine-rich (SFPQ) is a multifunctional nuclear RNA-binding protein (RBP) implicated in the regulation of gene expression pathways and intracellular trafficking. Here, we investigated the role of SFPQ in the regulation of the expression and function of F508del-CFTR in CF lung epithelial cells. We find that the expression of SFPQ is reduced in F508del-CFTR CF epithelial cells compared to WT-CFTR control cells. Interestingly, the overexpression of SFPQ in CF cells increases the expression as well as rescues the function of F508del-CFTR. Further, comprehensive transcriptome analyses indicate that SFPQ plays a key role in activating the mutant F508del-CFTR by modulating several cellular signaling pathways. This is the first report on the role of SFPQ in the regulation of expression and function of F508del-CFTR in CF lung disease. Our findings provide new insights into SFPQ-mediated molecular mechanisms and point to possible novel epigenetic therapeutic targets for CF and related pulmonary diseases.

Indexed as

BronchiCells, CulturedCystic FibrosisCystic Fibrosis Transmembrane Conductance RegulatorEpithelial CellsGene Expression RegulationHumansMutationPTB-Associated Splicing FactorTranscriptomeCFTR protein, humanCystic Fibrosis Transmembrane Conductance RegulatorPTB-Associated Splicing Factor

Identifiers

PMID34404863
PMCPMC8371023
OpenAlexW3195896608

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.