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

Store-operated Ca(2+) entry is not essential for PDGF-BB induced phenotype modulation in rat aortic smooth muscle.

Cell calcium - 1 Jul 2010

Emter Craig A, Bowles Douglas K

Abstract excerpt

Suppression of smooth muscle cell (SMC) differentiation marker genes is central to SMC phenotype modulation during vasculo-proliferative diseases such as atherosclerosis and restenosis. Upregulation of the intermediate-conductance Ca(2+)-activated K(+) channel (K(Ca)3.1) is integral for mitogen-induced suppression of SMC marker genes and post-angioplasty restenosis. Modulation of SMC marker gene expression has...

Read the complete abstract on PubMed

Topics

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

Share to Becaplermin
Share to Muscle, Smooth, Vascular
Share to Myocytes, Smooth Muscle

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Naphthalenes

Share to Platelet-Derived Growth Factor

Share to Proto-Oncogene Proteins c-sis

Share to Pyrones

Share to Rats, Sprague-Dawley

Source

Open in PubMed Open full text

Identifiers

PMID: 20619453
DOI: 10.1016/j.ceca.2010.06.001
PMCID: PMC2929302

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 6 Sept 2026. Manifest publication-graph-cohort-2026-09-06.1.

Source receipt: pubmed, retrieved 6 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Store-operated Ca(2+) entry is not essential for PDGF-BB induced phenotype modulation in rat aortic smooth muscle.PMID 20619453Read ↗

Upregulation of intermediate-conductance Ca2+-activated K+ channel (IKCa1) mediates phenotypic modulation of coronary smooth muscle.Semantic proximity Read ↗

Pyk2 inhibition promotes contractile differentiation in arterial smooth muscle.Semantic proximity Read ↗

Local delivery of the KCa3.1 blocker, TRAM-34, prevents acute angioplasty-induced coronary smooth muscle phenotypic modulation and limits stenosis.Semantic proximity Read ↗

Smoothelin is an indicator of reversible phenotype modulation of smooth muscle cells in balloon-injured rat carotid arteries.Semantic proximity Read ↗

Up-regulation of KCa3.1 promotes human airway smooth muscle cell phenotypic modulation.Semantic proximity Read ↗

PDGF-DD, a novel mediator of smooth muscle cell phenotypic modulation, is upregulated in endothelial cells exposed to atherosclerosis-prone flow patterns.Semantic proximity Read ↗

Changes in the balance of phosphoinositide 3-kinase/protein kinase B (Akt) and the mitogen-activated protein kinases (ERK/p38MAPK) determine a phenotype of visceral and vascular smooth muscle cells.Semantic proximity Read ↗

Ca2+ handling is altered when arterial myocytes progress from a contractile to a proliferative phenotype in culture.Semantic proximity Read ↗

Targeting connexin 43 prevents platelet-derived growth factor-BB-induced phenotypic change in porcine coronary artery smooth muscle cells.Semantic proximity Read ↗

[Effect of platelet-derived growth factor-BB on rat corpus cavernosum smooth muscle cell proliferation, migration and phenotypic modulation].Semantic proximity Read ↗

Phenotypic transformation of smooth muscle cells from porcine coronary arteries is associated with connexin 43.Semantic proximity Read ↗

[Effects of simvastatin on proliferation and transition of phenotype in PDGF-BB-induced pulmonary artery smooth muscle cells].Semantic proximity Read ↗

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