Evidence map›Paper›PMID 26440050›Full record

ArticleTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2016

Differential function and regulation of orphan nuclear receptor TR3 isoforms in endothelial cells.

Lei Zhou, Pengfei Cui, Shengqiang Zhao, Taiyang Ye, Yan Li, Jin Peng, Gengming Niu, Dezheng Zhao, Huiyan Zeng

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.1field-weighted citation impact, top 52% 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

1 citing paper in PubMed, 5 citations in OpenAlex.

  1. Article
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

9 authors at 6 institutions in 2 countries.

Lei ZhouCenter for Vascular Biology Research and Division of Molecular and Vascular Medicine, Department of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA, 02215, USA.
Pengfei CuiCenter for Vascular Biology Research and Division of Molecular and Vascular Medicine, Department of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA, 02215, USA.
Shengqiang ZhaoCenter for Vascular Biology Research and Division of Molecular and Vascular Medicine, Department of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA, 02215, USA.
Taiyang YeCenter for Vascular Biology Research and Division of Molecular and Vascular Medicine, Department of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA, 02215, USA.
Yan LiCenter for Vascular Biology Research and Division of Molecular and Vascular Medicine, Department of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA, 02215, USA.
Jin PengCenter for Vascular Biology Research and Division of Molecular and Vascular Medicine, Department of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA, 02215, USA.
Gengming NiuCenter for Vascular Biology Research and Division of Molecular and Vascular Medicine, Department of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA, 02215, USA.
Dezheng ZhaoCenter for Vascular Biology Research and Division of Molecular and Vascular Medicine, Department of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA, 02215, USA.
Huiyan ZengCenter for Vascular Biology Research and Division of Molecular and Vascular Medicine, Department of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA, 02215, USA. hzeng@bidmc.harvard.edu.
Beth Israel Deaconess Medical Center · USHarvard University · USCenter for Vascular Biology Research · USFudan University · CNRenji Hospital · CNZhongnan Hospital of Wuhan University · CN

Funding

Regulation of colitis by orphan nuclear receptor Nur77R01DK095873 · NIDDK · BETH ISRAEL DEACONESS MEDICAL CENTER · PI ZHAO, DEZHENG · 2013 to 2017
$1.9M
Orphan Nuclear Receptor TR3 in tumor angiogenesis and associated microvessel permR01CA133235 · NCI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI ZENG, HUIYAN · 2009 to 2013
$1.7M
Orphan nuclear receptor Nur77 and intestinal inflammmationR21DK080970 · NIDDK · BETH ISRAEL DEACONESS MEDICAL CENTER · PI ZHAO, DEZHENG · 2009 to 2010
$468k
NCI NIH HHS R01 CA133235NIDDK NIH HHS R01 DK095873NIDDK NIH HHS R21 DK080970
6 · The paper itself

Abstract

TR3 has been reported to be an excellent target for angiogenesis therapies. We reported three TR3 transcript variant messenger RNAs (mRNAs) are expressed in human umbilical vein endothelial cell (HUVEC) and are differentially regulated by vascular endothelial growth factor (VEGF). TR3 transcript variant 1 (TR3-TV1) and variant 2 (TR3-TV2) encoding the same TR3 isoform 1 protein (TR3-iso1) that was named TR3 has been extensively studied. However, the function of TR3 isoform 2 protein (TR3-iso2) encoded by TR3 transcript variant 3 (TR3-TV3) is still not known. Here, we clone and express the novel TR3-iso2 protein and find that expression of TR3-iso2, in contrast to TR3-iso1, inhibits endothelial cell proliferation induced by VEGF-A, histamine, and phorbol-12-myristate-13-acetate (PMA). The differential function of TR3-iso2 correlates with the down-regulation of cyclin D1. However, TR3-iso2 plays similar roles in endothelial cell migration and monolayer permeability as TR3-iso1. We further demonstrate that several intracellular signaling pathways are involved in histamine-induced TR3 transcript variants, including histamine receptor H1-mediated phospholipase C (PLC)/calcium /calcineurin/protein kinase C (PKC)/protein kinase D (PKD) pathway and ERK pathway, as well as histamine receptor H3-mediated PKC-ERK pathway. Further, expressions of TR3-TV1, TR3-TV2, and TR3-TV3 by VEGF and histamine are regulated by different promoters, but not by their mRNA stability.

Indexed as

Cell MovementCell ProliferationCells, CulturedGene ExpressionGene Expression ProfilingHistamineHumansHuman Umbilical Vein Endothelial CellsImmunoblottingNuclear Receptor Subfamily 4, Group A, Member 1Promoter Regions, GeneticProtein IsoformsReverse Transcriptase Polymerase Chain ReactionRNA InterferenceTetradecanoylphorbol AcetateVascular Endothelial Growth Factor AHistamineNuclear Receptor Subfamily 4, Group A, Member 1Protein IsoformsTetradecanoylphorbol AcetateVascular Endothelial Growth Factor AAngiogenesisCell proliferationCell signalingMigrationTR3/Nur77 transcription variants

Identifiers

PMID26440050
PMCPMC4837113
OpenAlexW2103423354

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.