Evidence map›Paper›PMID 26666517›Full record

ArticleBMC research notes2015

Whole-transcriptome gene expression profiling in an epidermolysis bullosa simplex Dowling-Meara model keratinocyte cell line uncovered novel, potential therapeutic targets and affected pathways.

Julia Herzog, Raphaela Rid, Martin Wagner, Harald Hundsberger, Andreas Eger, Johann Bauer, Kamil Önder

Abstract read
In one paragraph

Article in BMC research notes, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Review
  2. Keratins as an Inflammation Trigger Point in Epidermolysis Bullosa Simplex.International journal of molecular sciences · 2021
    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

7 authors.

Julia HerzogDivision of Molecular Dermatology, Department of Dermatology, Paracelsus Private Medical University Salzburg, Salzburg, Austria. j.herzog@salk.at.
Raphaela RidDivision of Molecular Dermatology, Department of Dermatology, Paracelsus Private Medical University Salzburg, Salzburg, Austria. r.rid@salk.at.
Martin WagnerDivision of Molecular Dermatology, Department of Dermatology, Paracelsus Private Medical University Salzburg, Salzburg, Austria. wagner.martin@sbg.at.
Harald HundsbergerDepartment of Medical and Pharmaceutical Biotechnology, University of Applied Sciences, Krems, Austria. harald.hundsberger@fh-krems.ac.at.
Andreas EgerDepartment of Medical and Pharmaceutical Biotechnology, University of Applied Sciences, Krems, Austria. andreas.eger@fh-krems.ac.at.
Johann BauerDivision of Molecular Dermatology, Department of Dermatology, Paracelsus Private Medical University Salzburg, Salzburg, Austria. jo.bauer@salk.at.
Kamil ÖnderDivision of Molecular Dermatology, Department of Dermatology, Paracelsus Private Medical University Salzburg, Salzburg, Austria. k.oender@salk.at.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundTo be able to develop effective therapeutics for epidermolysis bullosa simplex (EBS), it is necessary to elucidate the molecular pathomechanisms that give rise to the disease's characteristic severe skin-blistering phenotype.

resultsStarting with a whole-transcriptome microarray analysis of an EBS Dowling-Meara model cell line (KEB7), we identified 207 genes showing differential expression relative to control keratinocytes. A complementary qRT-PCR study of 156 candidates confirmed 76.58 % of the selected genes to be significantly up-regulated or down-regulated (p-value <0.05) within biological replicates. Our hit list contains previously identified genes involved in epithelial cell proliferation, cell-substrate adhesion, and responses to diverse biological stimuli. In addition, we identified novel candidate genes and potential affected pathways not previously considered as relevant to EBS pathology.

conclusionsOur results broaden our understanding of the molecular processes dysregulated in EBS.

Indexed as

Blotting, WesternCell LineEpidermolysis Bullosa SimplexGene Expression ProfilingGene OntologyGenetic Predisposition to DiseaseHumansKeratinocytesMolecular Targeted TherapyMutationOligonucleotide Array Sequence AnalysisReverse Transcriptase Polymerase Chain ReactionSignal TransductionTranscriptome

Identifiers

PMID26666517
PMCPMC4678661

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Registered trials

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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.