Evidence map›Paper›PMID 31337861›Full record

ArticleScientific reports2019

Transcriptomics of a KDELR1 knockout cell line reveals modulated cell adhesion properties.

Andrea Blum, Saleem Khalifa, Karl Nordström, Martin Simon, Marcel H Schulz, Manfred J Schmitt

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.2field-weighted citation impact, top 23% 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

9 citing papers in PubMed, 17 citations in OpenAlex.

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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

6 authors at 4 institutions in 1 country.

Andrea BlumMolecular and Cell Biology, Department of Biosciences (FR 8.3) and Center of Human and Molecular Biology (ZHMB), Saarland University, D-66123, Saarbrücken, Germany. andrea.blum@uni-saarland.de.
Saleem KhalifaCluster of Excellence, Multimodal Computing and Interaction, Saarland University and Department for Computational Biology and Applied Algorithmics, Max Planck Institute for Informatics, Saarland Informatics Campus, Saarbrücken, Germany.
Karl NordströmGenetics/Epigenetics, Center for Human and Molecular Biology, Saarland University, Saarbrücken, Germany.ORCID http://orcid.org/0000-0001-6231-4417
Martin SimonMolecular Cell Biology and Microbiology, Wuppertal University, D-42097, Wuppertal, Germany.
Marcel H SchulzCluster of Excellence, Multimodal Computing and Interaction, Saarland University and Department for Computational Biology and Applied Algorithmics, Max Planck Institute for Informatics, Saarland Informatics Campus, Saarbrücken, Germany.ORCID http://orcid.org/0000-0002-1252-3656
Manfred J SchmittMolecular and Cell Biology, Department of Biosciences (FR 8.3) and Center of Human and Molecular Biology (ZHMB), Saarland University, D-66123, Saarbrücken, Germany. mjs@microbiol.uni-sb.de.
Saarland University · DEGoethe University Frankfurt · DEMax Planck Institute for Informatics · DEUniversity of Wuppertal · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

KDEL receptors (KDELRs) represent transmembrane proteins of the secretory pathway which regulate the retention of soluble ER-residents as well as retrograde and anterograde vesicle trafficking. In addition, KDELRs are involved in the regulation of cellular stress response and ECM degradation. For a deeper insight into KDELR1 specific functions, we characterised a KDELR1-KO cell line (HAP1) through whole transcriptome analysis by comparing KDELR1-KO cells with its respective HAP1 wild-type. Our data indicate more than 300 significantly and differentially expressed genes whose gene products are mainly involved in developmental processes such as cell adhesion and ECM composition, pointing out to severe cellular disorders due to a loss of KDELR1. Impaired adhesion capacity of KDELR1-KO cells was further demonstrated through in vitro adhesion assays, while collagen- and/or laminin-coating nearly doubled the adhesion property of KDELR1-KO cells compared to wild-type, confirming a transcriptional adaptation to improve or restore the cellular adhesion capability. Perturbations within the secretory pathway were verified by an increased secretion of ER-resident PDI and decreased cell viability under ER stress conditions, suggesting KDELR1-KO cells to be severely impaired in maintaining cellular homeostasis.

Indexed as

Cell AdhesionCell LineCell MovementGene Expression ProfilingGene Knockout TechniquesHumansReceptors, PeptideSequence Analysis, DNAKDELR1 protein, humanReceptors, Peptide

Identifiers

PMID31337861
PMCPMC6650600
OpenAlexW2963579401

What OpenQuestion holds

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LicenceCC BY
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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.