Evidence map›Paper›PMID 27248291›Full record

ArticleSmall GTPases2017

Cdc42 regulates Cdc42EP3 function in cancer-associated fibroblasts.

Aaron J Farrugia, Fernando Calvo

Open access · hybridAbstract read
In one paragraph

Article in Small GTPases, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.9field-weighted citation impact, top 16% 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

22 citing papers in PubMed, 39 citations in OpenAlex.

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  19. CDC42 Negatively Regulates Testis-Specific SEPT12 Polymerization.International journal of molecular sciences · 2018
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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

2 authors at 1 institution in 1 country.

Aaron J Farrugiaa Tumour Microenvironment Team, Division of Cancer Biology , Institute of Cancer Research , London , UK.
Fernando Calvoa Tumour Microenvironment Team, Division of Cancer Biology , Institute of Cancer Research , London , UK.
Institute of Cancer Research · GB

Funding

Worldwide Cancer Research 15-0273
6 · The paper itself

Abstract

Rho family GTPases such as Cdc42 are key regulators of essential cellular processes through their effects on cytoskeletal dynamics, signaling and gene expression. Rho GTPases modulate these functions by engaging a wide variety of downstream effectors. Among these effectors is the largely understudied Cdc42EP/BORG family of Cdc42 effectors. BORG proteins have been linked to actin and septin regulation, but their role in development and disease is only starting to emerge. Recently, Cdc42EP3/BORG2 was shown to coordinate actin and septin cytoskeleton rearrangements in cancer-associated fibroblasts (CAFs). Interestingly, Cdc42EP3 expression potentiated cellular responses to mechanical stimulation leading to signaling and transcriptional adaptations required for the emergence of a fully activated CAF phenotype. These findings uncover a novel role for the BORG/septin network in cancer. Here, we demonstrate that Cdc42EP3 function in CAFs relies on tight regulation by Cdc42.

Indexed as

ActinsCancer-Associated Fibroblastscdc42 GTP-Binding ProteinGene Expression Regulation, NeoplasticGTP-Binding Protein RegulatorsHumansNeoplasmsSeptinsSignal TransductionActinsCDC42EP3 protein, humancdc42 GTP-Binding ProteinGTP-Binding Protein RegulatorsSeptinsBORGcancer-associated fibroblastsCdc42EP3cytoskeletonRho GTPasesseptin

Identifiers

PMID27248291
PMCPMC5331892
OpenAlexW2468314954

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.