Evidence map›Paper›PMID 23393131›Full record

Trial reportThe Journal of biological chemistry2013

Endothelial cell-specific chemotaxis receptor (ECSCR) enhances vascular endothelial growth factor (VEGF) receptor-2/kinase insert domain receptor (KDR) activation and promotes proteolysis of internalized KDR.

Sreenivasulu Kilari, Indulekha Remadevi, Baofeng Zhao, Jing Pan, Robert Miao, Ramani Ramchandran, Paula E North, Ming You, Nader Rahimi, George A Wilkinson

Open access · hybridAbstract readClinical Trial
In one paragraph

Trial report in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.7field-weighted citation impact, top 29% 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

11 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. MicroRNA-218-5p Promotes Endovascular Trophoblast Differentiation and Spiral Artery Remodeling.Molecular therapy : the journal of the American Society of Gene Therapy · 2018
    Article
  8. Article
  9. Article
  10. Article
  11. 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

10 authors at 3 institutions in 1 country.

Sreenivasulu KilariDepartment of Pediatrics and Developmental Vascular Biology Program, Medical College of Wisconsin and Children's Research Institute, Milwaukee, Wisconsin 53226, USA.
Indulekha Remadevi
Baofeng Zhao
Jing Pan
Robert Miao
Ramani Ramchandran
Paula E North
Ming You
Nader Rahimi
George A Wilkinson
Children's Hospital of Wisconsin · USMedical College of Wisconsin · USBoston University · US

Funding

Targeting DUSP-5 to Treat Vascular AnomaliesR01HL112639 · NHLBI · MEDICAL COLLEGE OF WISCONSIN · PI RAMCHANDRAN, RAMANI · 2012 to 2016
$2.6M
Role of NgBRR01HL108938 · NHLBI · MEDICAL COLLEGE OF WISCONSIN · PI MIAO, QING · 2011 to 2015
$1.8M
NHLBI NIH HHS R01 HL108938NHLBI NIH HHS R01 HL112639
6 · The paper itself

Abstract

The endothelial cell-specific chemotaxis receptor (ECSCR) is a cell-surface protein selectively expressed by endothelial cells (ECs), with roles in EC migration, apoptosis and proliferation. Our previous study (Verma, A., Bhattacharya, R., Remadevi, I., Li, K., Pramanik, K., Samant, G. V., Horswill, M., Chun, C. Z., Zhao, B., Wang, E., Miao, R. Q., Mukhopadhyay, D., Ramchandran, R., and Wilkinson, G. A. (2010) Blood 115, 4614-4622) showed that loss of ECSCR in primary ECs reduced tyrosine phosphorylation of vascular endothelial growth factor (VEGF) receptor 2/kinase insert domain receptor (KDR) but not VEGF receptor 1/FLT1. Here, we show that ECSCR biochemically associates with KDR but not FLT1 and that the predicted ECSCR cytoplasmic and transmembrane regions can each confer association with KDR. Stimulation with VEGF165 rapidly and transiently increases ECSCR-KDR complex formation, a process blocked by the KDR tyrosine kinase inhibitor compound SU5416 or inhibitors of endosomal acidification. Triple labeling experiments show VEGF-stimulated KDR(+)/ECSCR(+) intracellular co-localization. Silencing of ECSCR disrupts VEGF-induced KDR activation and AKT and ERK phosphorylation and impairs VEGF-stimulated KDR degradation. In zebrafish, ecscr interacts with kdrl during intersomitic vessel sprouting. Human placenta and infantile hemangioma samples highly express ECSCR protein, suggesting a role for ECSCR-KDR interaction in these tissues.

Indexed as

ProteolysisAnimalsAnimals, Genetically ModifiedApoptosis Regulatory ProteinsCell LineEndosomesEnzyme ActivationExtracellular Signal-Regulated MAP KinasesFemaleHemangiomaHumansHuman Umbilical Vein Endothelial CellsIndolesMaleMembrane ProteinsPlacentaApoptosis Regulatory ProteinsECSCR protein, humanExtracellular Signal-Regulated MAP KinasesFLT1 protein, humanIndolesMembrane ProteinsProtein Kinase InhibitorsProto-Oncogene Proteins c-aktPyrrolesSemaxinibVascular Endothelial Growth Factor Receptor-1Vascular Endothelial Growth Factor Receptor-2

Identifiers

PMID23393131
PMCPMC3624410
OpenAlexW2012950793

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.