Evidence map›Paper›PMID 18000534›Full record

ArticlePloS one2007

Neuropilin-1 modulates p53/caspases axis to promote endothelial cell survival.

Ling Wang, Shamit K Dutta, Tatsuyoshi Kojima, Xiaolei Xu, Roya Khosravi-Far, Stephen C Ekker, Debabrata Mukhopadhyay

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
3.6field-weighted citation impact, top 6% 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

40 citing papers in PubMed, 68 citations in OpenAlex.

  1. The Significance of Neuropilins in Gastrointestinal Cancers.International journal of molecular sciences · 2025
    Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Neuropilin-1 (NRP-1)/GIPC1 pathway mediates glioma progression.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
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  15. Review
  16. Review
  17. Article
  18. Article
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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 1 country.

Ling WangDepartment of Biochemistry and Molecular Biology, Mayo Clinic College of Medicine, Rochester, Minnesota, United States of America.
Shamit K Dutta
Tatsuyoshi Kojima
Xiaolei Xu
Roya Khosravi-Far
Stephen C Ekker
Debabrata Mukhopadhyay
Mayo Clinic · USHarvard University · USUniversity of Minnesota · US

Funding

Systematic Vertebrate Functional GenomicsR01GM063904 · NIGMS · UNIVERSITY OF TEXAS AT AUSTIN · PI EKKER, STEPHEN CARL · 2001 to 2025
$10.7M
Distinct Pathways of VPF/VEGF ReceptorsR01HL070567 · NHLBI · MAYO CLINIC ROCHESTER · PI MUKHOPADHYAY, DEBABRATA · 2002 to 2014
$4.7M
Regulatory Pathways and Role of VPF/VEGF in Renal CancerR01CA078383 · NCI · MAYO CLINIC ROCHESTER · PI MUKHOPADHYAY, DEBABRATA · 2004 to 2019
$4.5M
The Neurotransmitter dopamine and angiogenesisR01HL072178 · NHLBI · MAYO CLINIC ROCHESTER · PI MUKHOPADHYAY, DEBABRATA · 2003 to 2007
$1.5M
REGULATORY PATHWAYS AND ROLE OF VPF/VEGF IN RENAL CANCERR29CA078383 · NCI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI MUKHOPADHYAY, DEBABRATA · 1998 to 2002
$383k
NCI NIH HHS CA78383NCI NIH HHS R01 CA078383NCI NIH HHS R29 CA078383NHLBI NIH HHS HL072178NHLBI NIH HHS HL70567NHLBI NIH HHS R01 HL070567NHLBI NIH HHS R01 HL072178NIGMS NIH HHS R01 GM063904
6 · The paper itself

Abstract

Vascular permeability factor/vascular endothelial growth factor (VPF/VEGF), one of the crucial pro-angiogenic factors, functions as a potent inhibitor of endothelial cell (EC) apoptosis. Previous progress has been made towards delineating the VPF/VEGF survival signaling downstream of the activation of VEGFR-2. Here, we seek to define the function of NRP-1 in VPF/VEGF-induced survival signaling in EC and to elucidate the concomitant molecular signaling events that are pivotal for our understanding of the signaling of VPF/VEGF. Utilizing two different in vitro cell culture systems and an in vivo zebrafish model, we demonstrate that NRP-1 mediates VPF/VEGF-induced EC survival independent of VEGFR-2. Furthermore, we show here a novel mechanism for NRP-1-specific control of the anti-apoptotic pathway in EC through involvement of the NRP-1-interacting protein (NIP/GIPC) in the activation of PI-3K/Akt and subsequent inactivation of p53 pathways and FoxOs, as well as activation of p21. This study, by elucidating the mechanisms that govern VPF/VEGF-induced EC survival signaling via NRP-1, contributes to a better understanding of molecular mechanisms of cardiovascular development and disease and widens the possibilities for better therapeutic targets.

Indexed as

ApoptosisCaspasesCells, CulturedCell SurvivalEndothelium, VascularHumansNeuropilin-1Tumor Suppressor Protein p53Vascular Endothelial Growth Factor AVascular Endothelial Growth Factor Receptor-2CaspasesNeuropilin-1Tumor Suppressor Protein p53Vascular Endothelial Growth Factor AVascular Endothelial Growth Factor Receptor-2

Identifiers

PMID18000534
PMCPMC2048754
OpenAlexW2150027832

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.