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

Localization of c-Myb and induction of apoptosis by antisense oligonucleotide c-Myb after angioplasty of porcine coronary arteries.

Arteriosclerosis, thrombosis, and vascular biology - 1 Nov 2001

Lambert D L, Malik N, Shepherd L, Gunn J, Francis S E, King A, Crossman D C, Cumberland D C, Holt C M

Abstract excerpt

Previous studies have shown that inhibition of the proto-oncogene c-myb inhibits neointimal formation in various animal models. However, the temporal and spatial expression of c-Myb in the vessel wall after injury is not known, and the mechanism of action of antisense oligonucleotide (AS-ODN-c-myb) inhibition remains unclear. One potential effect of cell cycle dysregulation by inhibition of c-myb is an increase...

Read the complete abstract on PubMed

Topics

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

Share to Angioplasty, Balloon, Coronary
Share to Coronary Restenosis

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Coronary Vessels

Share to In Situ Nick-End Labeling

Share to Microscopy, Video

Share to Muscle, Smooth, Vascular

Share to Oligonucleotides, Antisense

Share to Proto-Oncogene Proteins c-myb

Source

Identifiers

PMID: 11701457
DOI: 10.1161/hq1101.098552

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Localization of c-Myb and induction of apoptosis by antisense oligonucleotide c-Myb after angioplasty of porcine coronary arteries.PMID 11701457Read ↗

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

MiR-140-3p is Involved in In-Stent Restenosis by Targeting C-Myb and BCL-2 in Peripheral Artery DiseaseSemantic proximity Read ↗

Injury-induced expression of cytokeratins 8 and 18 by vascular smooth muscle cells requires concurrent activation of cytoskeletal and growth factor receptors.Semantic proximity Read ↗

Attenuated herpes simplex virus 1 blocks arterial apoptosis and intimal hyperplasia induced by balloon angioplasty and reduced blood flow.Semantic proximity Read ↗

A decline in platelet activation and inflammatory cell infiltration is associated with the phenotypic redifferentiation of neointimal smooth muscle cells after bare-metal stent implantation in acute coronary syndrome.Semantic proximity Read ↗

The intron 6 G/T polymorphism of c-myb oncogene and the risk for coronary in-stent restenosis.Semantic proximity Read ↗

Resolution of apoptosis in atherosclerotic plaque by dietary modification and statin therapy.Semantic proximity Read ↗

Euonymine inhibits in-stent restenosis through enhancing contractile phenotype of vascular smooth muscle cells via modulating the PTEN/AKT/mTOR signaling pathway.Semantic proximity Read ↗

Dissociation of cardiomyocyte apoptosis and dedifferentiation in infarct border zonesSemantic proximity Read ↗

Inhibition of neointimal formation in porcine coronary artery by a Ras mutant.Semantic proximity Read ↗

Mutated p21/WAF/CIP transgene overexpression reduces smooth muscle cell proliferation, macrophage deposition, oxidation-sensitive mechanisms, and restenosis in hypercholesterolemic apolipoprotein E knockout mice.Semantic proximity Read ↗

Molecular mechanisms associated with the regulation of apoptosis by the two alternatively spliced products of c-Myb.Semantic proximity Read ↗

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