2015
PKCι interacts with Rab14 and modulates epithelial barrier function through regulation of claudin-2 levels
Lu R, Dalgalan D, Mandell EK, Parker SS, Ghosh S, Wilson JM. PKCι interacts with Rab14 and modulates epithelial barrier function through regulation of claudin-2 levels. Molecular Biology Of The Cell 2015, 26: 1523-1531. PMID: 25694446, PMCID: PMC4395131, DOI: 10.1091/mbc.e14-12-1613.Peer-Reviewed Original ResearchConceptsClaudin-2 levelsSmall GTPase Rab14Claudin-2 protein levelsClaudin-2Junction proteinsTransepithelial resistanceEpithelial polarityIntracellular punctaTight junction componentsTight junction proteinsPlasma membraneNormal assemblyRab14 expressionRab14Junction componentsPKCιKnockdownEpithelial barrier functionProtein levelsTight junctionsZO-1ProteinParacellular permeabilityClaudin-1APKC
2014
Local Translation and Retrograde Axonal Transport of CREB Regulates IL-6-Induced Nociceptive Plasticity
Melemedjian OK, Tillu DV, Moy JK, Asiedu MN, Mandell EK, Ghosh S, Dussor G, Price TJ. Local Translation and Retrograde Axonal Transport of CREB Regulates IL-6-Induced Nociceptive Plasticity. Molecular Pain 2014, 10: 1744-8069-10-45. PMID: 24993495, PMCID: PMC4091745, DOI: 10.1186/1744-8069-10-45.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAxonal TransportBrain-Derived Neurotrophic FactorCells, CulturedColchicineCREB-Binding ProteinDisease Models, AnimalGanglia, SpinalGene Expression RegulationInterleukin-6MaleMiceMice, Inbred ICRNociceptive PainNocodazoleProtein TransportQuinazolinonesSciatic NerveSensory Receptor CellsTubulin ModulatorsConceptsCyclic AMP response element binding proteinDorsal root gangliaInterleukin-6Retrograde axonal transportNerve growth factorHyperalgesic primingMechanical hypersensitivityAxonal transportNociceptive plasticitySensory neuronsRetrograde transportExpression of BDNFPrimary sensory neuronsExpression of CREBHr post injectionIL-6 treatmentAxonal traffickingActivity-dependent translationAMP response element binding proteinResponse element-binding proteinCREB DNA bindingIntrathecal injectionHindpaw injectionNociceptive sensitizationInflammatory model
2013
BDNF Regulates Atypical PKC at Spinal Synapses to Initiate and Maintain a Centralized Chronic Pain State
Melemedjian OK, Tillu DV, Asiedu MN, Mandell EK, Moy JK, Blute VM, Taylor CJ, Ghosh S, Price TJ. BDNF Regulates Atypical PKC at Spinal Synapses to Initiate and Maintain a Centralized Chronic Pain State. Molecular Pain 2013, 9: 1744-8069-9-12. PMID: 23510079, PMCID: PMC3608966, DOI: 10.1186/1744-8069-9-12.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBrain-Derived Neurotrophic FactorCalcium-Calmodulin-Dependent Protein Kinase Type 2Cerebral CortexChronic PainEukaryotic Initiation Factor-4FExtracellular Signal-Regulated MAP KinasesMaleMAP Kinase Signaling SystemMiceMice, Inbred ICRMitogen-Activated Protein Kinase KinasesModels, BiologicalPhosphorylationPosterior Horn CellsProtein BiosynthesisProtein Kinase CProtein TransportSynapsesTime FactorsTOR Serine-Threonine KinasesConceptsChronic pain statesPain statesPersistent nociceptive sensitizationSpinal synapsesChronic painNociceptive sensitizationPotential therapeutic targetImportant medical problemNeurotrophic factorBDNF regulationPersistent sensitizationBDNFTherapeutic targetMedical problemsPainNovel therapeuticsEssential mediatorSensitizationPermanent reversalSynapsesMolecular linkPKMζKey regulator