Evidence map›Paper›PMID 30781697›Full record

ArticleCells2019

RHOG Activates RAC1 through CDC42 Leading to Tube Formation in Vascular Endothelial Cells.

Oula El Atat, Amira Fakih, Mirvat El-Sibai

Open access · goldAbstract read
In one paragraph

Article in Cells, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

30 citing papers in PubMed, 38 citations in OpenAlex.

  1. Article
  2. Article
  3. Endothelial RhoGEF Trio is involved in angiogenesis.Vascular biology (Bristol, England) · 2026
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  19. RhoG-Rac1 Signaling Pathway Mediates Metabolic Dysfunction of the Pancreatic Beta-Cells Under Chronic Hyperglycemic Conditions.Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · 2021
    Article
  20. 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

3 authors at 1 institution in 1 country.

Oula El AtatDepartment of Natural Sciences, Lebanese American University, Beirut 1102 2801, Lebanon. oula.elatat@lau.edu.lb.
Amira FakihDepartment of Natural Sciences, Lebanese American University, Beirut 1102 2801, Lebanon. amira.fakih@lau.edu.lb.
Mirvat El-SibaiDepartment of Natural Sciences, Lebanese American University, Beirut 1102 2801, Lebanon. mirvat.elsibai@lau.edu.lb.
Lebanese American University · LB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Angiogenesis is a hallmark of cancer cell malignancy. The role of the RHO family GTPase RHOG in angiogenesis in vascular endothelial cells has recently been elucidated. However, the regulation of RHOG during this process, as well as its cross-talk with other RHO GTPases, have yet to be fully examined. In this study, we found that siRNA-mediated depletion of RHOG strongly inhibits tube formation in vascular endothelial cells (ECV cells), an effect reversed by transfecting dominant active constructs of CDC42 or RAC1 in the RHOG-depleted cells. We also found CDC42 to be upstream from RAC1 in these cells. Inhibiting either Phosphatidyl inositol (3) kinase (PI3K) with Wortmannin or the mitogen-activated protein kinase extracellular-regulated kinase (MAPK ERK) with U0126 leads to the inhibition of tube formation. While knocking down either RHO, GTPase did not affect p-AKT levels, and p-ERK decreased in response to the knocking down of RHOG, CDC42 or RAC1. Recovering active RHO GTPases in U0126-treated cells also did not reverse the inhibition of tube formation, placing ERK downstream from PI3K-RHOG-CDC42-RAC1 in vascular endothelial cells. Finally, RHOA and the Rho activated protein kinases ROCK1 and ROCK2 positively regulated tube formation independently of ERK, while RHOC seemed to inhibit the process. Collectively, our data confirmed the essential role of RHOG in angiogenesis, shedding light on a potential new therapeutic target for cancer malignancy and metastasis.

Indexed as

Neovascularization, Physiologiccdc42 GTP-Binding ProteinEndothelial CellsEnzyme ActivationHumansMAP Kinase Signaling SystemModels, BiologicalPhosphatidylinositol 3-Kinasesrac1 GTP-Binding Proteinrho GTP-Binding Proteinscdc42 GTP-Binding ProteinPhosphatidylinositol 3-Kinasesrac1 GTP-Binding ProteinRAC1 protein, humanRHOG protein, humanrho GTP-Binding ProteinsangiogenesisCDC42RAC1RHOGRHO GTPasesvascular endothelial cells

Identifiers

PMID30781697
PMCPMC6406863
OpenAlexW2914619929

What OpenQuestion holds

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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.