Evidence map›Paper›PMID 41760671›Full record

ArticleScientific reports2026

Large variations in total and allele-specific transcript expression in a disease mutation-independent manner.

Moritz Freyberg, Merete Bewig, Giovana Bavia Bampi, Candela Manfredi, Disha Joshi, Robert Rauscher, Jeong S Hong, Jörg Große-Onnebrink, Sivagurunathan Sutharsan, Florian Stehling and 4 more

Abstract read
In one paragraph

Article in Scientific reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

What it found

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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

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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

0 citing papers in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

14 authors.

Moritz Freyberg *Institute of Biochemistry and Molecular Biology, University of Hamburg, Hamburg, Germany.
Merete Bewig *Faculty of Medicine, Saarland University, Homburg, Germany.
Giovana Bavia Bampi *Institute of Biochemistry and Molecular Biology, University of Hamburg, Hamburg, Germany.
Candela ManfrediDepartment of Pediatrics, School of Medicine, Emory University, Atlanta, USA.
Disha JoshiDepartment of Pediatrics, School of Medicine, Emory University, Atlanta, USA.
Robert RauscherInstitute of Biochemistry and Molecular Biology, University of Hamburg, Hamburg, Germany.
Jeong S HongDepartment of Pediatrics, School of Medicine, Emory University, Atlanta, USA.
Jörg Große-OnnebrinkMünster University Hospital, Münster, Germany.
Sivagurunathan SutharsanDepartment of Pulmonary Medicine, Division of Cystic Fibrosis, University Medicine Essen-Ruhrlandklinik, University of Duisburg-Essen, Essen, Germany.
Florian StehlingPediatric Pulmonology University Hospital of Essen, Essen, Germany.
Ingrid BobisChristiane Herzog Zentrum Nord, Städtisches Krankenhaus Kiel, Kiel, Germany.
Manfred BallmannPediatric and Adolescence Clinic, University Medicine Rostock, Rostock, Germany. Manfred.Ballmann@med.uni-rostock.de.
Eric J SorscherDepartment of Pediatrics, School of Medicine, Emory University, Atlanta, USA. esorscher@emory.edu.
Zoya IgnatovaInstitute of Biochemistry and Molecular Biology, University of Hamburg, Hamburg, Germany. zoya.ignatova@uni-hamburg.de.

Funding

Ribosomal perturbation as a mechanism to prevent misfolding of CFTRR01HL136414 · NHLBI · EMORY UNIVERSITY · PI HARTMAN, JOHN L, SORSCHER, ERIC J · 2018 to 2025
$4.5M
NHLBI NIH HHS R01 HL136414
6 · The paper itself

Abstract

Individuals with monogenic diseases, even those with identical disease-causing mutations, exhibit considerable clinical heterogeneity in severity and outcomes. In this study, we quantified total and allele-specific transcript levels in nasal brushings from patients diagnosed with cystic fibrosis (CF) who are homozygous or compound heterozygous for variants in the cystic fibrosis transmembrane conductance regulator (CFTR) gene. Among CF patients, total CFTR transcript levels showed greater variability than in non-CF individuals, although both groups exhibited a broad range of transcript expression. Compound heterozygous study subjects also displayed notable differences in allelic dosage, known as allelic skewing. The expression from the non-F508del allele predominated in the total transcript pool. For a small group of patients with nasal brushings available before and after treatment with FDA/EMA-approved drugs Trikafta/Kaftrio (a combination of elexacaftor-tezacaftor-ivacaftor) or Symkevi (a combination of tezacaftor-ivacaftor), we observed no effect on total CFTR transcript abundance but detected changes in allelic expression patterns. These findings reveal important aspects to be considered for personalized therapeutic approaches to CF and other monogenic diseases and emphasize previously unappreciated aspects of mRNA expression during pathogenesis.

Indexed as

AllelesCystic FibrosisCystic Fibrosis Transmembrane Conductance RegulatorMutationAminophenolsBenzodioxolesDrug CombinationsHeterozygoteHumansIndolesPyrazolesPyridinesQuinolinesQuinolonesRNA, MessengerAminophenolsBenzodioxolesCFTR protein, humanCystic Fibrosis Transmembrane Conductance RegulatorDrug Combinationselexacaftor, ivacaftor, tezacaftor drug combinationIndolesPyrazolesPyridinesQuinolinesQuinolonesRNA, Messengertezacaftor, ivacaftor drug combinationAllele skewingCystic fibrosisGene expressionMonogenic diseasesmRNA

Identifiers

PMID41760671
PMCPMC12953693

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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.