Evidence map›Paper›PMID 29872538›Full record

ArticleCell discovery2018

Pseudopodium-enriched atypical kinase 1 mediates angiogenesis by modulating GATA2-dependent VEGFR2 transcription.

Huawei Wang, John Lapek, Ken Fujimura, Jan Strnadel, Bei Liu, David J Gonzalez, Wei Zhang, Felicia Watson, Vicky Yu, Chao Liu and 5 more

Open access · goldAbstract read
In one paragraph

Article in Cell discovery, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

16 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
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  4. Review
  5. EZH2 coordinates memory B-cell programming and recall responses.Journal of immunology (Baltimore, Md. : 1950) · 2025
    Article
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  16. SHEDding light on the role of Pragmin pseudo-kinases in cancer.American journal of cancer research · 2019
    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

15 authors at 2 institutions in 3 countries.

Huawei Wang1Department of Pathology, University of California San Diego, La Jolla, CA USA.ORCID 0000-0001-5481-303X
John Lapek3Department of Pharmacology, University of California San Diego, La Jolla, CA USA.
Ken Fujimura1Department of Pathology, University of California San Diego, La Jolla, CA USA.
Jan Strnadel1Department of Pathology, University of California San Diego, La Jolla, CA USA.
Bei Liu1Department of Pathology, University of California San Diego, La Jolla, CA USA.
David J Gonzalez3Department of Pharmacology, University of California San Diego, La Jolla, CA USA.
Wei Zhang5Department of Medicine, University of California San Diego, La Jolla, CA USA.ORCID 0000-0002-0942-1245
Felicia Watson1Department of Pathology, University of California San Diego, La Jolla, CA USA.
Vicky Yu1Department of Pathology, University of California San Diego, La Jolla, CA USA.
Chao Liu5Department of Medicine, University of California San Diego, La Jolla, CA USA.
Carina Muccilo Melo6Department of Biochemistry, Universidade Federal de São Paulo, São Paulo/SP, Brazil.
Yury I Miller5Department of Medicine, University of California San Diego, La Jolla, CA USA.
Kathryn C Elliott1Department of Pathology, University of California San Diego, La Jolla, CA USA.
David A Cheresh1Department of Pathology, University of California San Diego, La Jolla, CA USA.
Richard L Klemke1Department of Pathology, University of California San Diego, La Jolla, CA USA.
University of California San Diego · USUniversidade Federal de São Paulo · BR

Funding

UCSD/SDSU IRACDAK12GM068524 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI TREJO, JOANN · 2003 to 2025
$24.4M
AIBP therapyR35HL135737 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI MILLER, YURY · 2017 to 2023
$6.5M
VEGF and PDGF in angiogenesis and tumor progressionR37CA050286 · NCI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI CHERESH, DAVID A · 1999 to 2013
$6.3M
Survival Mechanisms of Invasive Carcinoma CellsR01CA097022 · NCI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI KLEMKE, RICHARD L. · 2003 to 2017
$4.6M
Fingerprinting Invasive Membrane Protrusions to Discover Metastatic SignaturesR01CA182495 · NCI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI KLEMKE, RICHARD L. · 2014 to 2024
$3.9M
STRUCTURAL AND FUNCTIONAL STUDIES--INTEGERIN-DEPENDENTR01CA050286 · NCI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI CHERESH, DAVID A · 1989 to 2018
$1.9M
Vascular communication in metastatic brain colonizationR01CA184594 · NCI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI KLEMKE, RICHARD L. · 2014 to 2018
$1.6M
Deciphering the Role of eIF5A/PEAK1 Pathway in Pancreatic CancerF32CA180374 · NCI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI FUJIMURA, KEN · 2013 to 2015
$171k
NCI NIH HHS F32 CA180374NCI NIH HHS R01 CA050286NCI NIH HHS R01 CA097022NCI NIH HHS R01 CA182495NCI NIH HHS R01 CA184594NCI NIH HHS R37 CA050286NHLBI NIH HHS R35 HL135737NIGMS NIH HHS K12 GM068524
6 · The paper itself

Abstract

PEAK1 is a newly described tyrosine kinase and scaffold protein that transmits integrin-mediated extracellular matrix (ECM) signals to facilitate cell movement and growth. While aberrant expression of PEAK1 has been linked to cancer progression, its normal physiological role in vertebrate biology is not known. Here we provide evidence that PEAK1 plays a central role in orchestrating new vessel formation in vertebrates. Deletion of the PEAK1 gene in zebrafish, mice, and human endothelial cells (ECs) induced severe defects in new blood vessel formation due to deficiencies in EC proliferation, survival, and migration. Gene transcriptional and proteomic analyses of PEAK1-deficient ECs revealed a significant loss of vascular endothelial growth factor receptor 2 (VEGFR2) mRNA and protein expression, as well as downstream signaling to its effectors, ERK, Akt, and Src kinase. PEAK1 regulates VEGFR2 expression by binding to and increasing the protein stability of the transcription factor GATA-binding protein 2 (GATA2), which controls VEGFR2 transcription. Importantly, PEAK1-GATA2-dependent VEGFR2 expression is mediated by EC adhesion to the ECM and is required for breast cancer-induced new vessel formation in mice. Also, elevated expression of PEAK1 and VEGFR2 mRNA are highly correlated in many human cancers including breast cancer. Together, our findings reveal a novel PEAK1-GATA2-VEGFR2 signaling axis that integrates cell adhesion and growth factor cues from the extracellular environment necessary for new vessel formation during vertebrate development and cancer.

Identifiers

PMID29872538
PMCPMC5972149
OpenAlexW2806077988

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Registered trials

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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.