Evidence map›Paper›PMID 24585635›Full record

ArticleJournal of cellular physiology2014

ERK3 promotes endothelial cell functions by upregulating SRC-3/SP1-mediated VEGFR2 expression.

Wei Wang, Ka Bian, Sreeram Vallabhaneni, Bin Zhang, Ray-Chang Wu, Bert W O'Malley, Weiwen Long

Open access · greenAbstract read
In one paragraph

Article in Journal of cellular physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
1.3field-weighted citation impact, top 22% 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

27 citing papers in PubMed, 42 citations in OpenAlex.

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  12. A steroid receptor coactivator stimulator (MCB-613) attenuates adverse remodeling after myocardial infarction.Proceedings of the National Academy of Sciences of the United States of America · 2020
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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

7 authors at 3 institutions in 2 countries.

Wei WangDepartment of Molecular and Cellular Biology, Baylor College of Medicine, One Baylor Plaza, Houston, Texas.
Ka Bian
Sreeram Vallabhaneni
Bin Zhang
Ray-Chang Wu
Bert W O'Malley
Weiwen Long
Baylor College of Medicine · USGeorge Washington University · USWright State University · US

Funding

REPRODUCTIVE HORMONES: BIOLOGICAL AND MOLECULAR ACTIONSR01HD008188 · NICHD · BAYLOR COLLEGE OF MEDICINE · PI DAVID M LONARD, JOHN P LYDON · 1985 to 2026
$16.3M
SEX HORMONE RECEPTOR COMPONENTS AND THE CELL GENOMER01HD007857 · NICHD · BAYLOR COLLEGE OF MEDICINE · PI DAVID M LONARD, JOHN P LYDON · 1985 to 2026
$14.6M
SEX HORMONE RECEPTOR COMPONENTS &THE CELL GENOMER37HD007857 · NICHD · BAYLOR COLLEGE OF MEDICINE · PI MC KEOWN, MICHAEL B · 1987 to 1996
–
NICHD NIH HHS 5R01HD-8188NICHD NIH HHS HD07857NICHD NIH HHS R01 HD007857NICHD NIH HHS R01 HD008188
6 · The paper itself

Abstract

Despite a regain of interest recently in ERK3 kinase signaling, the molecular regulations of both ERK3 gene expression and protein kinase activity are still largely unknown. While it is shown that disruption of ERK3 gene causes neonatal lethality, cell type-specific functions of ERK3 signaling remain to be explored. In this study, we report that ERK3 gene expression is upregulated by cytokines through c-Jun in endothelial cells; c-Jun binds to the ERK3 gene and regulates its transcription. We further reveal a new role for ERK3 in regulating endothelial cell migration, proliferation and tube formation by upregulating SRC-3/SP-1-mediated VEGFR2 expression. The underlying molecular mechanism involves ERK3-stimulated formation of a transcriptional complex involving coactivator SRC-3, transcription factor SP-1 and the secondary coactivator CBP. Taken together, our study identified a molecular regulatory mechanism of ERK3 gene expression and revealed a previously unknown role of ERK3 in regulating endothelial cell functions.

Indexed as

Neovascularization, PhysiologicBinding SitesCell MovementCell ProliferationCREB-Binding ProteinGene Expression Regulation, EnzymologicHeLa CellsHumansHuman Umbilical Vein Endothelial CellsMitogen-Activated Protein Kinase 6Nuclear Receptor Coactivator 3Promoter Regions, GeneticRNA InterferenceSignal TransductionSp1 Transcription FactorTime FactorsCREB-Binding ProteinCREBBP protein, humanKDR protein, humanMitogen-Activated Protein Kinase 6NCOA3 protein, humanNuclear Receptor Coactivator 3Sp1 Transcription FactorTumor Necrosis Factor-alphaVascular Endothelial Growth Factor Receptor-2

Identifiers

PMID24585635
PMCPMC4078721
OpenAlexW1903984126

What OpenQuestion holds

Textmetadata
LicenceTDM
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.