2012
Endothelial Nuclear Factor-&kgr;B–Dependent Regulation of Arteriogenesis and Branching
Tirziu D, Jaba IM, Yu P, Larrivée B, Coon BG, Cristofaro B, Zhuang ZW, Lanahan AA, Schwartz MA, Eichmann A, Simons M. Endothelial Nuclear Factor-&kgr;B–Dependent Regulation of Arteriogenesis and Branching. Circulation 2012, 126: 2589-2600. PMID: 23091063, PMCID: PMC3514045, DOI: 10.1161/circulationaha.112.119321.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAnimals, NewbornBecaplerminBrainDisease Models, AnimalEndothelial CellsHindlimbHuman Umbilical Vein Endothelial CellsHumansHypoxia-Inducible Factor 1, alpha SubunitIschemiaMiceMice, TransgenicNeovascularization, PathologicNeovascularization, PhysiologicNF-kappa B p50 SubunitProto-Oncogene Proteins c-sisRetinaVascular Endothelial Growth Factor AConceptsNuclear factor-κB activationCollateral formationReduced adhesion molecule expressionHypoxia-inducible factor-1α levelsDistal tissue perfusionVascular endothelial growth factorAdhesion molecule expressionPlatelet-derived growth factor-BBEndothelial growth factorGrowth factor-BBMolecule expressionMonocyte influxCollateral networkTissue perfusionImmature vesselsArterial networkBaseline levelsNFκB activationNuclear factorFactor-BBGrowth factor
2007
Synectin‐dependent suppression of basal Rac1 activity is reversed by a signaling pathway involving PKCalpha and RhoG
Elfenbein A, Simons M. Synectin‐dependent suppression of basal Rac1 activity is reversed by a signaling pathway involving PKCalpha and RhoG. The FASEB Journal 2007, 21: lb11-lb12. DOI: 10.1096/fasebj.21.6.lb11-d.Peer-Reviewed Original ResearchFibroblast growth factorEndothelial cellsHigh-affinity tyrosine kinase receptorsLow baseline levelsRac1 activitySerum-starved endothelial cellsHigh-affinity receptorTyrosine kinase receptorsBaseline levelsGrowth factorInhibitor-1Endothelial cell migrationHeparan sulfate proteoglycanDissociation inhibitor 1Kinase receptorsMigratory responseEarly eventsNovel roleSulfate proteoglycanCell migration