Evidence map›Paper›PMID 24703491›Full record

ArticleMolecular genetics and metabolism2014

Transcriptional profiling of the human fibrillin/LTBP gene family, key regulators of mesenchymal cell functions.

Margaret R Davis, Robin Andersson, Jessica Severin, Michiel de Hoon, Nicolas Bertin, J Kenneth Baillie, Hideya Kawaji, Albin Sandelin, Alistair R R Forrest, Kim M Summers and 1 more

Open access · hybridAbstract read
In one paragraph

Article in Molecular genetics and metabolism, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.0field-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

23 citing papers in PubMed, 38 citations in OpenAlex.

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  19. Recapitulating and Correcting Marfan Syndrome in a Cellular Model.International journal of biological sciences · 2017
    Article
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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

11 authors at 4 institutions in 4 countries.

Margaret R DavisThe Roslin Institute and Royal (Dick) School of Veterinary Studies, University of Edinburgh, Easter Bush EH25 9RG, UK. Electronic address: margaret.davis@roslin.ed.ac.uk.
Robin AnderssonThe Bioinformatics Centre, Department of Biology and Biotech Research and Innovation Centre, University of Copenhagen, Ole Maaloes Vej 5, 2200 Copenhagen N, Denmark. Electronic address: robin@binf.ku.dk.
Jessica SeverinRIKEN Omics Science Center, Yokohama, Kanagawa 230-0045, Japan(1); RIKEN Center for Life Science Technologies, Division of Genomic Technologies, Yokohama, Kanagawa 230-0045, Japan. Electronic address: severin@gsc.rkien.jp.
Michiel de HoonRIKEN Omics Science Center, Yokohama, Kanagawa 230-0045, Japan(1); RIKEN Center for Life Science Technologies, Division of Genomic Technologies, Yokohama, Kanagawa 230-0045, Japan. Electronic address: mdehoon@gsc.riken.jp.
Nicolas BertinRIKEN Omics Science Center, Yokohama, Kanagawa 230-0045, Japan(1); RIKEN Center for Life Science Technologies, Division of Genomic Technologies, Yokohama, Kanagawa 230-0045, Japan. Electronic address: nbertin@gsc.riken.jp.
J Kenneth BaillieThe Roslin Institute and Royal (Dick) School of Veterinary Studies, University of Edinburgh, Easter Bush EH25 9RG, UK. Electronic address: kennethbaillie@gmail.com.
Hideya KawajiRIKEN Omics Science Center, Yokohama, Kanagawa 230-0045, Japan(1); RIKEN Center for Life Science Technologies, Division of Genomic Technologies, Yokohama, Kanagawa 230-0045, Japan; RIKEN Preventive Medicine and Diagnosis Innovation Program, Wako, Saitama 351-0198, Japan. Electronic address: kawaji@gsc.riken.jp.
Albin SandelinThe Bioinformatics Centre, Department of Biology and Biotech Research and Innovation Centre, University of Copenhagen, Ole Maaloes Vej 5, 2200 Copenhagen N, Denmark. Electronic address: albin@binf.ku.dk.
Alistair R R ForrestRIKEN Omics Science Center, Yokohama, Kanagawa 230-0045, Japan(1); RIKEN Center for Life Science Technologies, Division of Genomic Technologies, Yokohama, Kanagawa 230-0045, Japan. Electronic address: forrest@gsc.riken.jp.
Kim M SummersThe Roslin Institute and Royal (Dick) School of Veterinary Studies, University of Edinburgh, Easter Bush EH25 9RG, UK; The University of Queensland Northside Clinical School, Prince Charles Hospital, Chermside 4032, Australia. Electronic address: kim.summers@roslin.ed.ac.uk.
FANTOM Consortium
University of Copenhagen · DKUniversity of Edinburgh · GBRIKEN · JPRoslin Institute · GB

Funding

Biotechnology and Biological Sciences Research Council BB/I024801/1Biotechnology and Biological Sciences Research Council BBS/E/D/20211552Wellcome Trust
6 · The paper itself

Abstract

The fibrillins and latent transforming growth factor binding proteins (LTBPs) form a superfamily of extracellular matrix (ECM) proteins characterized by the presence of a unique domain, the 8-cysteine transforming growth factor beta (TGFβ) binding domain. These proteins are involved in the structure of the extracellular matrix and controlling the bioavailability of TGFβ family members. Genes encoding these proteins show differential expression in mesenchymal cell types which synthesize the extracellular matrix. We have investigated the promoter regions of the seven gene family members using the FANTOM5 CAGE database for human. While the protein and nucleotide sequences show considerable sequence similarity, the promoter regions were quite diverse. Most genes had a single predominant transcription start site region but LTBP1 and LTBP4 had two regions initiating different transcripts. Most of the family members were expressed in a range of mesenchymal and other cell types, often associated with use of alternative promoters or transcription start sites within a promoter in different cell types. FBN3 was the lowest expressed gene, and was found only in embryonic and fetal tissues. The different promoters for one gene were more similar to each other in expression than to promoters of the other family members. Notably expression of all 22 LTBP2 promoters was tightly correlated and quite distinct from all other family members. We located candidate enhancer regions likely to be involved in expression of the genes. Each gene was associated with a unique subset of transcription factors across multiple promoters although several motifs including MAZ, SP1, GTF2I and KLF4 showed overrepresentation across the gene family. FBN1 and FBN2, which had similar expression patterns, were regulated by different transcription factors. This study highlights the role of alternative transcription start sites in regulating the tissue specificity of closely related genes and suggests that this important class of extracellular matrix proteins is subject to subtle regulatory variations that explain the differential roles of members of this gene family.

Indexed as

Gene Expression ProfilingAdipokinesCell LineEnhancer Elements, GeneticExtracellular MatrixFibrillin-1Fibrillin-2FibrillinsHumansKruppel-Like Factor 4Latent TGF-beta Binding ProteinsMesenchymal Stem CellsMicrofilament ProteinsMultigene FamilyOrgan SpecificityPromoter Regions, GeneticAdipokinesFBN1 protein, humanFBN2 protein, humanFibrillin-1Fibrillin-2FibrillinsKLF4 protein, humanKruppel-Like Factor 4Latent TGF-beta Binding ProteinsMicrofilament ProteinsExtracellular matrixFibrillinGene regulationLatent transforming growth factor β binding proteinPromoterTranscription start sites

Identifiers

PMID24703491
PMCPMC4019825
OpenAlexW2099499053

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.