Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

ARF GTPases control phenotypic switching of vascular smooth muscle cells through the regulation of actin function and actin dependent gene expression.

Cellular signalling - 1 Jun 2018

Charles Ricardo, Bourmoum Mohamed, Claing Audrey

Abstract excerpt

Vascular smooth muscle cells (VSMC) can exhibit a contractile or a synthetic phenotype depending on the extracellular stimuli present and the composition of the extracellular matrix. Uncontrolled activation of the synthetic VSMC phenotype is however associated with the development of cardiovascular diseases. Here, we aimed to elucidate the role of the ARF GTPases in the regulation of VSMC dedifferentiation....

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Actin Cytoskeleton
Share to ADP-Ribosylation Factor 1

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to ADP-Ribosylation Factor 6

Share to ADP-Ribosylation Factors

Share to Muscle Contraction

Share to Myocytes, Smooth Muscle

Share to Stress Fibers

Share to Triazoles

Source

Identifiers

PMID: 29499306
DOI: 10.1016/j.cellsig.2018.02.012

Genes

ARF1
ARF6

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 3 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

ARF GTPases control phenotypic switching of vascular smooth muscle cells through the regulation of actin function and actin dependent gene expression.PMID 29499306Read ↗

ARF6 controls VSMC cell phenotypic switching upon lipid stimulation to promote inflammatory signaling contributing to the progression of atherosclerosisSemantic proximity Read ↗

ARF6 controls VSMC phenotypic switching upon lipid stimulation to promote inflammatory signaling contributing to the progression of atherosclerosis.Semantic proximity Read ↗

Molecular mechanisms of phenotypic plasticity in smooth muscle cells.Semantic proximity Read ↗

Transcriptional regulation of vascular smooth muscle cell proliferation, differentiation and senescence: Novel targets for therapy.Semantic proximity Read ↗

Role of RhoA and Rho-associated kinase in phenotypic switching of vascular smooth muscle cells: Implications for vascular function.Semantic proximity Read ↗

Integrin α9 regulates smooth muscle cell phenotype switching and vascular remodeling.Semantic proximity Read ↗

IQGAP1 promotes the phenotypic switch of vascular smooth muscle by myocardin pathway: a potential target for varicose vein.Semantic proximity Read ↗

Smooth Muscle-Alpha Actin Inhibits Vascular Smooth Muscle Cell Proliferation and Migration by Inhibiting Rac1 Activity.Semantic proximity Read ↗

Control of phenotypic plasticity of smooth muscle cells by bone morphogenetic protein signaling through the myocardin-related transcription factors.Semantic proximity Read ↗

Intracellular Ca²⁺ signalling and phenotype of vascular smooth muscle cells.Semantic proximity Read ↗

Regulatory mechanism of human vascular smooth muscle cell phenotypic transformation induced by NELIN.Semantic proximity Read ↗

Deficiency of protein inhibitor of activated STAT3 exacerbates atherosclerosis by modulating VSMC phenotypic switching.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.