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