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David J. Loskutoff
Researcher at Scripps Research Institute
Publications - 235
Citations - 23807
David J. Loskutoff is an academic researcher from Scripps Research Institute. The author has contributed to research in topics: Plasminogen activator & Plasminogen activator inhibitor-1. The author has an hindex of 87, co-authored 235 publications receiving 23316 citations. Previous affiliations of David J. Loskutoff include VU University Amsterdam & Scripps Health.
Papers
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Journal ArticleDOI
Monocyte chemoattractant protein 1 in obesity and insulin resistance
Peter Sartipy,David J. Loskutoff +1 more
TL;DR: The results suggest that elevated MCP-1 may induce adipocyte dedifferentiation and contribute to pathologies associated with hyperinsulinemia and obesity, including type II diabetes.
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Endothelial cells produce a latent inhibitor of plasminogen activators that can be activated by denaturants.
TL;DR: Analysis of treated and untreated conditioned medium by gel filtration revealed that the latent and active PAIs migrated with apparent Mr values of 30,000 and 50,000, respectively, which indicate that the two PAIs are immunologically related and suggest thatThe latent form is converted into the active form by the sodium dodecyl sulfate present during the purification.
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Increased type 1 plasminogen activator inhibitor gene expression in atherosclerotic human arteries.
Jacob Schneiderman,Michael Sawdey,M. Keeton,Gerald M. Bordin,Eugene F. Bernstein,Ralph B. Dilley,David J. Loskutoff +6 more
TL;DR: Examination of the expression of PAI-1 mRNA in segments of 11 severely diseased and 5 relatively normal human arteries obtained from 16 different patients undergoing reconstructive surgery for aortic occlusive or aneurysmal disease provides initial evidence for the increased expression and suggests a role for PAi-1 in the progression of human atherosclerotic disease.
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Cytokine activation of vascular endothelium. Effects on tissue-type plasminogen activator and type 1 plasminogen activator inhibitor.
TL;DR: The fact that both rIL-1 beta and rTNF alpha act in a similar manner strengthens the hypothesis that the local development of inflammatory/immune processes could reduce endothelial fibrinolytic activity.
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Is plasminogen activator inhibitor-1 the molecular switch that governs urokinase receptor-mediated cell adhesion and release?
TL;DR: A dynamic regulatory role for PAI-1 and uPA in uPAR-mediated cell adhesion and release is suggested, and may help to explain why high PAi-1 levels indicate a poor prognosis for many cancers.