2016
The Robo4 cytoplasmic domain is dispensable for vascular permeability and neovascularization
Zhang F, Prahst C, Mathivet T, Pibouin-Fragner L, Zhang J, Genet G, Tong R, Dubrac A, Eichmann A. The Robo4 cytoplasmic domain is dispensable for vascular permeability and neovascularization. Nature Communications 2016, 7: 13517. PMID: 27882935, PMCID: PMC5123080, DOI: 10.1038/ncomms13517.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCapillary PermeabilityDiabetic RetinopathyIntercellular Signaling Peptides and ProteinsMiceMice, KnockoutNeovascularization, PathologicNerve Tissue ProteinsNetrin ReceptorsOxygen Inhalation TherapyPhosphorylationReceptors, Cell SurfaceReceptors, ImmunologicRetinal DiseasesRetinopathy of PrematuritySignal TransductionVascular Endothelial Growth Factor Receptor-2Wound HealingConceptsCytoplasmic domainOxygen-induced retinopathyVascular permeabilityRetinopathy of prematurityTransmembrane receptorsWound healingDiabetic wound healingCutaneous wound healingDiabetic patientsUNC5B receptorRobo4Transgenic miceTissue revascularizationRevascularizationVessel permeabilityRetinopathyMiceHealingNeovascularizationReceptorsDomainPhosphorylationDeletionPrematurityPathway
2013
Angiopoietin-2 Secretion by Endothelial Cell Exosomes REGULATION BY THE PHOSPHATIDYLINOSITOL 3-KINASE (PI3K)/Akt/ENDOTHELIAL NITRIC OXIDE SYNTHASE (eNOS) AND SYNDECAN-4/SYNTENIN PATHWAYS*
Ju R, Zhuang ZW, Zhang J, Lanahan AA, Kyriakides T, Sessa WC, Simons M. Angiopoietin-2 Secretion by Endothelial Cell Exosomes REGULATION BY THE PHOSPHATIDYLINOSITOL 3-KINASE (PI3K)/Akt/ENDOTHELIAL NITRIC OXIDE SYNTHASE (eNOS) AND SYNDECAN-4/SYNTENIN PATHWAYS*. Journal Of Biological Chemistry 2013, 289: 510-519. PMID: 24235146, PMCID: PMC3879572, DOI: 10.1074/jbc.m113.506899.Peer-Reviewed Original ResearchConceptsPI3K/Akt/endothelial nitric oxide synthaseAkt/endothelial nitric oxide synthaseAkt1 null miceCritical signaling pathwaysMode of secretionEndothelial nitric oxide synthaseExtracellular proteinsSignaling pathwaysSyndecan-4Angiopoietin/Tie2Novel mechanismVascular defectsNitric oxide synthaseAngiopoietin-2 secretionNull miceTie2 receptorPathwayPrincipal ligandEndothelial cellsSynthaseVascular integrityRegulationOxide synthaseVascular growthImportant role