Evidence map›Paper›PMID 25870111›Full record

ArticleMolecular and cellular biology2015

SMAD1 and SMAD5 Expression Is Coordinately Regulated by FLI1 and GATA2 during Endothelial Development.

Jonathon Marks-Bluth, Anchit Khanna, Vashe Chandrakanthan, Julie Thoms, Thomas Bee, Christina Eich, Young Chan Kang, Kathy Knezevic, Qiao Qiao, Simon Fitch and 5 more

Open access · bronzeAbstract read
In one paragraph

Article in Molecular and cellular biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.8field-weighted citation impact, top 28% 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

10 citing papers in PubMed, 14 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. 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

15 authors at 8 institutions in 5 countries.

Jonathon Marks-BluthLowy Cancer Research Centre and the Prince of Wales Clinical School, The University of New South Wales, Sydney, NSW, Australia The Weatherall Institute of Molecular Medicine, University of Oxford, Oxford, United Kingdom.
Anchit KhannaLowy Cancer Research Centre and the Prince of Wales Clinical School, The University of New South Wales, Sydney, NSW, Australia.
Vashe ChandrakanthanLowy Cancer Research Centre and the Prince of Wales Clinical School, The University of New South Wales, Sydney, NSW, Australia.
Julie ThomsLowy Cancer Research Centre and the Prince of Wales Clinical School, The University of New South Wales, Sydney, NSW, Australia.
Thomas BeeLowy Cancer Research Centre and the Prince of Wales Clinical School, The University of New South Wales, Sydney, NSW, Australia.
Christina EichErasmus MC Stem Cell Institute, Department of Cell Biology, Erasmus University Medical Center, Rotterdam, Netherlands.
Young Chan KangLowy Cancer Research Centre and the Prince of Wales Clinical School, The University of New South Wales, Sydney, NSW, Australia.
Kathy KnezevicLowy Cancer Research Centre and the Prince of Wales Clinical School, The University of New South Wales, Sydney, NSW, Australia.
Qiao QiaoLowy Cancer Research Centre and the Prince of Wales Clinical School, The University of New South Wales, Sydney, NSW, Australia.
Simon FitchDepartment of Haematology, Cambridge Institute for Medical Research, University of Cambridge, Cambridge, United Kingdom Cambridge Stem Cell Institute, University of Cambridge, Cambridge, United Kingdom.
Leif OxburghCenter for Molecular Medicine, Maine Medical Center Research Institute, Scarborough, Maine, USA.
Katrin OttersbachDepartment of Haematology, Cambridge Institute for Medical Research, University of Cambridge, Cambridge, United Kingdom Cambridge Stem Cell Institute, University of Cambridge, Cambridge, United Kingdom.
Elaine DzierzakErasmus MC Stem Cell Institute, Department of Cell Biology, Erasmus University Medical Center, Rotterdam, Netherlands The Queen's Medical Research Institute, College of Medicine and Veterinary Medicine, Edinburgh, United Kingdom.
Marella F T R de BruijnThe Weatherall Institute of Molecular Medicine, University of Oxford, Oxford, United Kingdom marella.debruijn@imm.ox.ac.uk jpimanda@unsw.edu.au.
John E PimandaLowy Cancer Research Centre and the Prince of Wales Clinical School, The University of New South Wales, Sydney, NSW, Australia Department of Haematology, Prince of Wales Hospital, Sydney, NSW, Australia marella.debruijn@imm.ox.ac.uk jpimanda@unsw.edu.au.
UNSW Sydney · AUUniversity of Oxford · GBErasmus MC Cancer Institute · NLMaine Medical Center · USPrince of Wales Hospital · AUQueen's University · CAUniversity of Cambridge · GBWellcome/MRC Cambridge Stem Cell Institute · GB

Funding

Characterization of the first HSCs during mouse ontogenyR37DK054077 · NIDDK · UNIVERSITY OF EDINBURGH · PI DZIERZAK, ELAINE A · 2006 to 2015
$2.7M
Medical Research Council MC_UU_12009/2NIDDK NIH HHS R37 DK054077NIDDK NIH HHS R37DK054077Wellcome Trust 97922
6 · The paper itself

Abstract

The bone morphogenetic protein (BMP)/SMAD signaling pathway is a critical regulator of angiogenic sprouting and is involved in vascular development in the embryo. SMAD1 and SMAD5, the core mediators of BMP signaling, are vital for this activity, yet little is known about their transcriptional regulation in endothelial cells. Here, we have integrated multispecies sequence conservation, tissue-specific chromatin, in vitro reporter assay, and in vivo transgenic data to identify and validate Smad1+63 and the Smad5 promoter as tissue-specific cis-regulatory elements that are active in the developing endothelium. The activity of these elements in the endothelium was dependent on highly conserved ETS, GATA, and E-box motifs, and chromatin immunoprecipitation showed high levels of enrichment of FLI1, GATA2, and SCL at these sites in endothelial cell lines and E11 dorsal aortas in vivo. Knockdown of FLI1 and GATA2 but not SCL reduced the expression of SMAD1 and SMAD5 in endothelial cells in vitro. In contrast, CD31(+) cKit(-) endothelial cells harvested from embryonic day 9 (E9) aorta-gonad-mesonephros (AGM) regions of GATA2 null embryos showed reduced Smad1 but not Smad5 transcript levels. This is suggestive of a degree of in vivo selection where, in the case of reduced SMAD1 levels, endothelial cells with more robust SMAD5 expression have a selective advantage.

Indexed as

Gene Expression Regulation, DevelopmentalAnimalsBase SequenceCell LineEndotheliumGATA2 Transcription FactorGene Knockdown TechniquesMiceMolecular Sequence DataPromoter Regions, GeneticProto-Oncogene Protein c-fli-1Smad1 ProteinSmad5 ProteinFli1 protein, mouseGata2 protein, mouseGATA2 Transcription FactorProto-Oncogene Protein c-fli-1Smad1 ProteinSmad5 Protein

Identifiers

PMID25870111
PMCPMC4438244
OpenAlexW2110833302

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.