Evidence map›Paper›PMID 32506201›Full record

ArticleAngiogenesis2020

RHOQ is induced by DLL4 and regulates angiogenesis by determining the intracellular route of the Notch intracellular domain.

Esther Bridges, Helen Sheldon, Esther Kleibeuker, Evelyn Ramberger, Christos Zois, Alun Barnard, Ulrike Harjes, Ji-Liang Li, Massimo Masiero, Robert MacLaren and 1 more

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Angiogenesis, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

20 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Notch Signaling in the Vasculature: Angiogenesis and Angiocrine Functions.Cold Spring Harbor perspectives in medicine · 2023
    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

11 authors at 2 institutions in 1 country.

Esther BridgesCancer Research UK Department of Medical Oncology, Weatherall Institute of Molecular Medicine, University of Oxford, Oxford, OX3 9DS, UK.ORCID 0000-0002-6958-6279
Helen SheldonCancer Research UK Department of Medical Oncology, Weatherall Institute of Molecular Medicine, University of Oxford, Oxford, OX3 9DS, UK.
Esther KleibeukerCancer Research UK Department of Medical Oncology, Weatherall Institute of Molecular Medicine, University of Oxford, Oxford, OX3 9DS, UK.
Evelyn RambergerCancer Research UK Department of Medical Oncology, Weatherall Institute of Molecular Medicine, University of Oxford, Oxford, OX3 9DS, UK.
Christos ZoisCancer Research UK Department of Medical Oncology, Weatherall Institute of Molecular Medicine, University of Oxford, Oxford, OX3 9DS, UK.
Alun BarnardOxford Eye Hospital, University of Oxford, Oxford, OX3 9DS, UK.
Ulrike HarjesCancer Research UK Department of Medical Oncology, Weatherall Institute of Molecular Medicine, University of Oxford, Oxford, OX3 9DS, UK.
Ji-Liang LiCancer Research UK Department of Medical Oncology, Weatherall Institute of Molecular Medicine, University of Oxford, Oxford, OX3 9DS, UK.
Massimo MasieroCancer Research UK Department of Medical Oncology, Weatherall Institute of Molecular Medicine, University of Oxford, Oxford, OX3 9DS, UK.
Robert MacLarenOxford Eye Hospital, University of Oxford, Oxford, OX3 9DS, UK.
Adrian HarrisCancer Research UK Department of Medical Oncology, Weatherall Institute of Molecular Medicine, University of Oxford, Oxford, OX3 9DS, UK. adrian.harris@oncology.ox.ac.uk.
Cancer Research UK · GBUniversity of Oxford · GB

Funding

Cancer Research UK 18974Cancer Research UK No. C602/A18974
6 · The paper itself

Abstract

Angiogenesis, the formation of new blood vessels by endothelial cells, is a finely tuned process relying on the balance between promoting and repressing signalling pathways. Among these, Notch signalling is critical in ensuring appropriate response of endothelial cells to pro-angiogenic stimuli. However, the downstream targets and pathways effected by Delta-like 4 (DLL4)/Notch signalling and their subsequent contribution to angiogenesis are not fully understood. We found that the Rho GTPase, RHOQ, is induced by DLL4 signalling and that silencing RHOQ results in abnormal sprouting and blood vessel formation both in vitro and in vivo. Loss of RHOQ greatly decreased the level of Notch signalling, conversely overexpression of RHOQ promoted Notch signalling. We describe a new feed-forward mechanism regulating DLL4/Notch signalling, whereby RHOQ is induced by DLL4/Notch and is essential for the NICD nuclear translocation. In the absence of RHOQ, Notch1 becomes targeted for degradation in the autophagy pathway and NICD is sequestered from the nucleus and targeted for degradation in lysosomes.

Indexed as

Neovascularization, PhysiologicSignal TransductionAdaptor Proteins, Signal TransducingCalcium-Binding ProteinsHumansHuman Umbilical Vein Endothelial CellsProtein DomainsReceptors, Notchrho GTP-Binding ProteinsAdaptor Proteins, Signal TransducingCalcium-Binding ProteinsDLL4 protein, humanReceptors, Notchrho GTP-Binding ProteinsRHOQ protein, humanAngiogenesisAutophagy pathwayDLL4 Notch1 signallingNICD degradationRHOQ

Identifiers

PMID32506201
PMCPMC7311507
OpenAlexW3033825380

What Socratic 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 Socratic graph.