2019
Epithelial (E)-Cadherin is a Novel Mediator of Platelet Aggregation and Clot Stability
Scanlon VM, Teixeira AM, Tyagi T, Zou S, Zhang PX, Booth CJ, Kowalska MA, Bao J, Hwa J, Hayes V, Marks MS, Poncz M, Krause DS. Epithelial (E)-Cadherin is a Novel Mediator of Platelet Aggregation and Clot Stability. Thrombosis And Haemostasis 2019, 119: 744-757. PMID: 30861547, PMCID: PMC6599679, DOI: 10.1055/s-0039-1679908.Peer-Reviewed Original ResearchConceptsConditional knockout miceKnockout micePlatelet aggregationE-cadherinClot stabilityClot stabilizationSynthase kinase 3β activationAntibody-mediated platelet depletionVivo injury modelsNull plateletsPlatelet productionWild-type miceTail bleeding timeAkt/GSK3βMurine platelet aggregationKnockout mouse modelPlatelet dysfunctionFibrin depositionInjury modelPlatelet depletionPrimary human plateletsBleeding timeMouse modelPlatelet numberE-cadherin antibody
2016
Loss of Cbl-PI3K interaction modulates the periosteal response to fracture by enhancing osteogenic commitment and differentiation
Scanlon V, Walia B, Yu J, Hansen M, Drissi H, Maye P, Sanjay A. Loss of Cbl-PI3K interaction modulates the periosteal response to fracture by enhancing osteogenic commitment and differentiation. Bone 2016, 95: 124-135. PMID: 27884787, PMCID: PMC5819877, DOI: 10.1016/j.bone.2016.11.020.Peer-Reviewed Original ResearchMeSH KeywordsAlkaline PhosphataseAnimalsBiomarkersCell CountCell DifferentiationCell LineageCell NucleusCell ProliferationFracture HealingFractures, BoneMesodermMice, Inbred C57BLMutationOsteogenesisPeriosteumPhosphatidylinositol 3-KinasePhosphorylationProtein BindingProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-cblSp7 Transcription FactorUp-RegulationConceptsCbl-PI3K interactionUbiquitin ligase functionMultipotent skeletal progenitorsPeriosteal cellsPI3KMajor adaptor proteinP85 regulatory subunitTranscriptional target genesE3 ubiquitin ligaseOsteogenic differentiationPhosphatidylinositol-3 kinasePI3K regulationMajor signaling proteinsK interactionPI3K activityPeriosteal thickeningLipid kinasesP85 subunitSkeletal progenitorsAdaptor proteinRegulatory subunitLigase functionSignaling proteinsUbiquitin ligaseNuclear localization
2015
Role of Cbl-PI3K Interaction during Skeletal Remodeling in a Murine Model of Bone Repair
Scanlon V, Soung do Y, Adapala NS, Morgan E, Hansen MF, Drissi H, Sanjay A. Role of Cbl-PI3K Interaction during Skeletal Remodeling in a Murine Model of Bone Repair. PLOS ONE 2015, 10: e0138194. PMID: 26393915, PMCID: PMC4578922, DOI: 10.1371/journal.pone.0138194.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBone RemodelingMiceMice, Inbred C57BLModels, AnimalPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-cblConceptsCbl-PI3K interactionHistomorphometric analysisFracture callusBone formationMid-diaphyseal femoral fracturePI3KNormal bone homeostasisBony callus formationSoft callus formationHealing femursFemoral fracturesWT miceOsteoclast numberBone resorptionTomography scanMurine modelOsteoblast surfaceFracture healingBone homeostasisBone volumeBone repairSkeletal remodelingMiceBiomechanical testingHigh expression