Evidence map›Paper›PMID 27852824›Full record

ArticleThe Journal of biological chemistry2016

Differential Receptor Binding and Regulatory Mechanisms for the Lymphangiogenic Growth Factors Vascular Endothelial Growth Factor (VEGF)-C and -D.

Natalia Davydova, Nicole C Harris, Sally Roufail, Sophie Paquet-Fifield, Musarat Ishaq, Victor A Streltsov, Steven P Williams, Tara Karnezis, Steven A Stacker, Marc G Achen

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.8field-weighted citation impact, top 8% 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

19 citing papers in PubMed, 40 citations in OpenAlex.

  1. Article
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  4. Structure-Based Design of Peptides Targeting VEGF/VEGFRs.Pharmaceuticals (Basel, Switzerland) · 2023
    Review
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  12. Observational
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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

10 authors at 3 institutions in 1 country.

Natalia DavydovaFrom the Tumour Angiogenesis and Microenvironment Program, Peter MacCallum Cancer Centre, Melbourne, Victoria 3000.
Nicole C HarrisFrom the Tumour Angiogenesis and Microenvironment Program, Peter MacCallum Cancer Centre, Melbourne, Victoria 3000.
Sally RoufailFrom the Tumour Angiogenesis and Microenvironment Program, Peter MacCallum Cancer Centre, Melbourne, Victoria 3000.
Sophie Paquet-FifieldFrom the Tumour Angiogenesis and Microenvironment Program, Peter MacCallum Cancer Centre, Melbourne, Victoria 3000.
Musarat IshaqFrom the Tumour Angiogenesis and Microenvironment Program, Peter MacCallum Cancer Centre, Melbourne, Victoria 3000.
Victor A Streltsovthe Florey Institute of Neuroscience and Mental Health, 30 Royal Parade, Parkville, Victoria 3052, and.
Steven P WilliamsFrom the Tumour Angiogenesis and Microenvironment Program, Peter MacCallum Cancer Centre, Melbourne, Victoria 3000.
Tara KarnezisFrom the Tumour Angiogenesis and Microenvironment Program, Peter MacCallum Cancer Centre, Melbourne, Victoria 3000.
Steven A StackerFrom the Tumour Angiogenesis and Microenvironment Program, Peter MacCallum Cancer Centre, Melbourne, Victoria 3000.
Marc G AchenFrom the Tumour Angiogenesis and Microenvironment Program, Peter MacCallum Cancer Centre, Melbourne, Victoria 3000, marc.achen@petermac.org.
Peter MacCallum Cancer Centre · AUFlorey Institute of Neuroscience and Mental Health · AUUniversity of Melbourne · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

VEGF-C and VEGF-D are secreted glycoproteins that induce angiogenesis and lymphangiogenesis in cancer, thereby promoting tumor growth and spread. They exhibit structural homology and activate VEGFR-2 and VEGFR-3, receptors on endothelial cells that signal for growth of blood vessels and lymphatics. VEGF-C and VEGF-D were thought to exhibit similar bioactivities, yet recent studies indicated distinct signaling mechanisms (e.g. tumor-derived VEGF-C promoted expression of the prostaglandin biosynthetic enzyme COX-2 in lymphatics, a response thought to facilitate metastasis via the lymphatic vasculature, whereas VEGF-D did not). Here we explore the basis of the distinct bioactivities of VEGF-D using a neutralizing antibody, peptide mapping, and mutagenesis to demonstrate that the N-terminal α-helix of mature VEGF-D (Phe

Indexed as

LymphangiogenesisAnimalsAntibodies, NeutralizingCells, CulturedDermisEndothelium, VascularFemaleHumansLymphatic VesselsMice, Inbred NODMice, SCIDMutagenesis, Site-DirectedMutationNeovascularization, PathologicSignal TransductionVascular Endothelial Growth Factor CAntibodies, NeutralizingVascular Endothelial Growth Factor CVascular Endothelial Growth Factor DVascular Endothelial Growth Factor Receptor-2Vascular Endothelial Growth Factor Receptor-3VEGFC protein, humanVEGFD protein, humanangiogenesisendothelial celllymphangiogenesismutagenesis in vitroreceptorvascular endothelial growth factor (VEGF)

Identifiers

PMID27852824
PMCPMC5207153
OpenAlexW2550383888

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.