Evidence map›Paper›PMID 29416084›Full record

ArticleScientific reports2018

Nuclear FAK and its kinase activity regulate VEGFR2 transcription in angiogenesis of adult mice.

Shaogang Sun, Hsin-Jung Wu, Jun-Lin Guan

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
4.8field-weighted citation impact, top 4% 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

33 citing papers in PubMed, 58 citations in OpenAlex.

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  12. New Insights on the Nuclear Functions and Targeting of FAK in Cancer.International journal of molecular sciences · 2022
    Review
  13. FAK in Cancer: From Mechanisms to Therapeutic Strategies.International journal of molecular sciences · 2022
    Review
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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

3 authors at 1 institution in 1 country.

Shaogang SunDepartments of Cancer Biology, University of Cincinnati College of Medicine, Cincinnati, OH, 45267, USA.
Hsin-Jung WuDepartments of Cancer Biology, University of Cincinnati College of Medicine, Cincinnati, OH, 45267, USA.
Jun-Lin GuanDepartments of Cancer Biology, University of Cincinnati College of Medicine, Cincinnati, OH, 45267, USA. guanjl@uc.edu.
University of Cincinnati Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Focal adhesion kinase (FAK) is essential in embryonic angiogenesis by regulating endothelial cell (EC) survival and barrier functions through its kinase-independent and -dependent activities. Here, we generated EC-specific tamoxifen-inducible FAK knockout and FAK kinase-defective (KD) mutant knockin mice to investigate the role of FAK and its kinase activity in angiogenesis of adult animals. Unlike previous observations of their differential defects in embryonic vascular development, both FAK ablation and inactivation of its kinase activity resulted in deficient angiogenesis in wound-healing as well as retinal angiogenesis models. Consistent with these phenotypes, loss of FAK or its kinase activity decreased EC proliferation and migration to similar extents, suggesting FAK primarily acts as a kinase for the regulation of adult EC-mediated angiogenesis. Further mechanistic analyses were carried out using an established mouse EC line MS1 cells. Interestingly, we found that FAK regulated the expression of VEGFR2, a central mediator of various EC functions and angiogenesis, which requires both FAK kinase activity and its translocation into the nucleus. Moreover, nuclear FAK was detected in the RNA polymerase II complex associated with VEGFR2 promoter, suggesting its direct participation in the transcriptional regulation of VEGFR2. Together, our results provide significant insights into the signaling mechanisms of FAK in angiogenesis that may contribute to future design of more effective angiogenesis related therapy.

Indexed as

Transcription, GeneticAnimalsCell MovementCell NucleusCell ProliferationCells, CulturedDisease Models, AnimalEndothelial CellsFemaleFocal Adhesion Kinase 1Gene Expression RegulationMaleMiceMice, Inbred C57BLRetinal NeovascularizationSignal TransductionFocal Adhesion Kinase 1Kdr protein, mousePtk2 protein, mouseVascular Endothelial Growth Factor Receptor-2

Identifiers

PMID29416084
PMCPMC5803223
OpenAlexW2805611044

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.