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

NO attenuates insulin signaling and motility in aortic smooth muscle cells via protein tyrosine phosphatase 1B-mediated mechanism.

Arteriosclerosis, thrombosis, and vascular biology - 1 Jul 2002

Sreejayan Nair, Lin Yi, Hassid Aviv

Abstract excerpt

OBJECTIVE: Hyperinsulinemia is a significant risk factor for the pathogenesis of vascular disease. Protein tyrosine phosphatase 1B (PTP1B) has been recognized as a modulator of insulin signaling in nonvascular cells, and we have recently reported that NO increases the activity of PTP1B in rat vascular smooth muscle cells. In the present study, we tested the hypothesis that NO attenuates insulin-stimulated cell...

Read the complete abstract on PubMed

Topics

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

Share to Aorta, Thoracic
Share to Butadienes
Share to Mitogen-Activated Protein Kinase 1

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Mitogen-Activated Protein Kinase 3

Share to Nitric Oxide Donors

Share to Phosphotyrosine

Share to Protein Tyrosine Phosphatase, Non-Receptor Type 1

Share to src Homology Domains

Source

Identifiers

PMID: 12117721
DOI: 10.1161/01.atv.0000020550.65963.e9

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

NO attenuates insulin signaling and motility in aortic smooth muscle cells via protein tyrosine phosphatase 1B-mediated mechanism.PMID 12117721Read ↗

Chronic insulin treatment amplifies PDGF-induced motility in differentiated aortic smooth muscle cells by suppressing the expression and function of PTP1B.Semantic proximity Read ↗

Deletion of Protein Tyrosine Phosphatase 1B (PTP1B) Enhances Endothelial Cyclooxygenase 2 Expression and Protects Mice from Type 1 Diabetes-Induced Endothelial Dysfunction.Semantic proximity Read ↗

Insulin-stimulated cyclic guanosine monophosphate inhibits vascular smooth muscle cell migration by inhibiting Ca/calmodulin-dependent protein kinase II.Semantic proximity Read ↗

Effect of endothelium-specific insulin resistance on endothelial function in vivo.Semantic proximity Read ↗

Adiponectin stimulates production of nitric oxide in vascular endothelial cells.Semantic proximity Read ↗

Insulin receptor substrate-1 and phosphoinositide-dependent kinase-1 are required for insulin-stimulated production of nitric oxide in endothelial cells.Semantic proximity Read ↗

Protein tyrosine phosphatase 1B, a major regulator of leptin-mediated control of cardiovascular function.Semantic proximity Read ↗

Insulin affects vascular smooth muscle cell phenotype and migration via distinct signaling pathways.Semantic proximity Read ↗

Nitric oxide-induced motility in aortic smooth muscle cells: role of protein tyrosine phosphatase SHP-2 and GTP-binding protein Rho.Semantic proximity Read ↗

Phenotypic changes in vascular smooth muscle cells during aging: insulin effect on migration.Semantic proximity Read ↗

Altered phosphodiesterase 3-mediated cAMP hydrolysis contributes to a hypermotile phenotype in obese JCR:LA-cp rat aortic vascular smooth muscle cells: implications for diabetes-associated cardiovascular disease.Semantic proximity Read ↗

Endothelial nitric oxide synthase is involved in calcium-induced Akt signaling in mouse skeletal muscle.Semantic proximity Read ↗

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