Search results for "PDZ Domains"

showing 2 items of 2 documents

MiR-33a Controls hMSCS Osteoblast Commitment Modulating the Yap/Taz Expression Through EGFR Signaling Regulation

2019

Mesenchymal stromal cells (hMSCs) display a pleiotropic function in bone regeneration. The signaling involved in osteoblast commitment is still not completely understood, and that determines the failure of current therapies being used. In our recent studies, we identified two miRNAs as regulators of hMSCs osteoblast differentiation driving hypoxia signaling and cytoskeletal reorganization. Other signalings involved in this process are epithelial to mesenchymal transition (EMT) and epidermal growth factor receptor (EGFR) signalings through the regulation of Yes-associated protein (YAP)/PDZ-binding motif (TAZ) expression. In the current study, we investigated the role of miR-33a family as a (…

epithelial mesenchymal transitionregenerative medicinePDZ DomainsCell CommunicationArticlemicroRNAmedicineHumansEpidermal growth factor receptorEpithelial–mesenchymal transitionBone regenerationCells CulturedEGFR inhibitorsAdaptor Proteins Signal TransducingOsteoblastsmicroRNAbiologyMesenchymal stem cellComputational BiologyOsteoblastMesenchymal Stem CellsYAP-Signaling ProteinsGeneral MedicinePhenotypeCell biologymicroRNAsErbB Receptorsmedicine.anatomical_structureTranscriptional Coactivator with PDZ-Binding Motif Proteinsmesenchymal stromal cellbiology.proteinTrans-Activatorsmesenchymal stromal cellsEGFR signalingSignal TransductionTranscription FactorsCells
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PTEN recruitment controls synaptic and cognitive function in Alzheimer's models

2016

Dyshomeostasis of amyloid-β peptide (Aβ) is responsible for synaptic malfunctions leading to cognitive deficits ranging from mild impairment to full-blown dementia in Alzheimer's disease. Aβ appears to skew synaptic plasticity events toward depression. We found that inhibition of PTEN, a lipid phosphatase that is essential to long-term depression, rescued normal synaptic function and cognition in cellular and animal models of Alzheimer's disease. Conversely, transgenic mice that overexpressed PTEN displayed synaptic depression that mimicked and occluded Aβ-induced depression. Mechanistically, Aβ triggers a PDZ-dependent recruitment of PTEN into the postsynaptic compartment. Using a PTEN kno…

0301 basic medicinePrimary Cell CulturePDZ DomainsMice TransgenicMolecular neuroscienceBiologyNeurotransmissionSynaptic TransmissionMice03 medical and health sciences0302 clinical medicineAlzheimer DiseasePostsynaptic potentialmedicineAnimalsPTENGene Knock-In TechniquesAmyloid beta-PeptidesGeneral NeurosciencePTEN PhosphohydrolaseLong-term potentiationmedicine.diseaseRatsDisease Models Animal030104 developmental biologySynaptic fatigueSynaptic plasticitybiology.proteinAlzheimer's diseaseCognition DisordersNeuroscience030217 neurology & neurosurgeryNature Neuroscience
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