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

Effects of dominant-negative c-Jun on platelet-derived growth factor-induced vascular smooth muscle cell proliferation.

Arteriosclerosis, thrombosis, and vascular biology - 1 Jan 2002

Zhan Yumei, Kim Shokei, Yasumoto Hideo, Namba Masashi, Miyazaki Hitoshi, Iwao Hiroshi

Abstract excerpt

Although platelet-derived growth factor (PDGF)-BB is thought to participate in vascular disorders, the mechanism of PDGF-induced vascular smooth muscle cell (SMC) proliferation is not fully understood. This study was undertaken to examine the role of c-Jun in PDGF-BB-induced proliferation of rat aortic SMCs. PDGF-BB (10 ng/mL) significantly increased activator protein (AP)-1 DNA binding activity in SMCs, followed...

Read the complete abstract on PubMed

Topics

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

Share to Becaplermin
Share to G1 Phase

Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Share to Muscle, Smooth, Vascular

Share to Platelet-Derived Growth Factor

Share to Proto-Oncogene Proteins c-jun

Share to Proto-Oncogene Proteins c-sis

Share to Receptors, Platelet-Derived Growth Factor

Share to Transcription Factor AP-1

Source

Identifiers

PMID: 11788465
DOI: 10.1161/hq0102.101821

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence. Graph snapshot: 2026-09-29.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Effects of dominant-negative c-Jun on platelet-derived growth factor-induced vascular smooth muscle cell proliferation.PMID 11788465Read ↗

The platelet-derived growth factor controls c-myc expression through a JNK- and AP-1-dependent signaling pathway.Semantic proximity Read ↗

Overexpression of mutated IkappaBalpha inhibits vascular smooth muscle cell proliferation and intimal hyperplasia formation.Semantic proximity Read ↗

Regulation of vascular smooth muscle cell proliferation: role of NF-kappaB revisited.Semantic proximity Read ↗

Platelet-derived growth factor (PDGF) receptor-alpha activates c-Jun NH2-terminal kinase-1 and antagonizes PDGF receptor-beta -induced phenotypic transformation.Semantic proximity Read ↗

PDGF-BB enhances alpha1beta1 integrin-mediated activation of the ERK/AP-1 pathway involved in collagen matrix remodeling by rat mesangial cells.Semantic proximity Read ↗

p27(Kip1) and p21(Cip1)-independent proliferative inhibition of vascular smooth muscle cells cultured in type-I collagen matrix honeycombs.Semantic proximity Read ↗

Dominant-negative mutant of c-Jun gene transfer: a novel therapeutic strategy for colorectal cancer.Semantic proximity Read ↗

Sp1 inhibits proliferation and induces apoptosis in vascular smooth muscle cells by repressing p21WAF1/Cip1 transcription and cyclin D1-Cdk4-p21WAF1/Cip1 complex formation.Semantic proximity Read ↗

Mechanism of action of a dominant-negative mutant of c-Jun.Semantic proximity Read ↗

Dominant negative mutant of c-Jun inhibits cardiomyocyte hypertrophy induced by endothelin 1 and phenylephrine.Semantic proximity Read ↗

Stress and vascular responses: mitogen-activated protein kinases and activator protein-1 as promising therapeutic targets of vascular remodeling.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 ↗

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