2025
Autism-like atypical face processing in Shank3 mutant dogs
Yuan S, Pang C, Wu L, Yi L, Guo K, Jiang Y, Zhang Y, Han S. Autism-like atypical face processing in Shank3 mutant dogs. Science Advances 2025, 11: eadu3793. PMID: 40173245, PMCID: PMC11963970, DOI: 10.1126/sciadv.adu3793.Peer-Reviewed Original ResearchConceptsAtypical face processingAutism spectrum disorderFace processingCategorization of facesFace processing abilitiesWild-type controlsAttentional avoidanceNeurocognitive basisSocial deficitsCognitive markersTemporal cortexASD mechanismsSpectrum disorderNeural responsesFrontal/parietal regionsProcessing abilityAnimal modelsEffective animal modelRisk genesCortical responsesGenetic associationAutismFaceCortexSHANK3Long-Term Engraftment of Cryopreserved Human Neurons for In Vivo Disease Modeling in Neurodegenerative Disease
Marmion D, Deng P, Hiller B, Lewis R, Harms L, Cameron D, Nolta J, Kordower J, Fink K, Wakeman D. Long-Term Engraftment of Cryopreserved Human Neurons for In Vivo Disease Modeling in Neurodegenerative Disease. Biology 2025, 14: 217. PMID: 40001985, PMCID: PMC11852092, DOI: 10.3390/biology14020217.Peer-Reviewed Original ResearchCentral nervous systemStriatum of Sprague-Dawley ratsForebrain GABAergic neuronsLong-term engraftmentHuman induced pluripotent stem cellsHuman neuronsSprague-Dawley ratsWild-type controlsPluripotent stem cellsPrefrontal cortexMature neuronal phenotypeRNU ratsHost striatumDisease in vivoGABAergic neuronsPost-transplantationImmunodeficient ratsIn vivo disease modelsIGABAHuntington's diseaseCynomolgus monkeysNeuronal phenotypeHD miceCNS environmentNeuronal survivalDeletion of sphingosine 1-phosphate receptor 1 in myeloid cells reduces hepatic inflammatory macrophages and attenuates MASH
Parthasarathy G, Venkatesan N, Sidhu G, Song M, Liao C, Barrow F, Mauer A, Sehrawat T, Nakao Y, Daniel P, Dasgupta D, Pavelko K, Revelo X, Malhi H. Deletion of sphingosine 1-phosphate receptor 1 in myeloid cells reduces hepatic inflammatory macrophages and attenuates MASH. Hepatology Communications 2025, 9: e0613. PMID: 39899672, DOI: 10.1097/hc9.0000000000000613.Peer-Reviewed Original ResearchConceptsMyeloid cellsMonocyte-derived macrophagesHigh-fatLiver injuryProinflammatory monocyte-derived macrophagesReceptor 1Cell-specific knockout miceMass cytometryT cell subsetsSphingosine 1-phosphate receptor 1Cardiometabolic risk factorsS1P receptor 1Accumulation of monocyte-derived macrophagesImmune cell typesWild-typeLiver inflammatory infiltrationGene ontology pathway analysisWild-type controlsDevelopment of steatohepatitisSphingosine 1-phosphateMitogen-activated protein kinase pathwayT cellsIntrahepatic macrophagesInflammatory infiltrateKnockout mice
2024
Aging-dependent loss of functional connectivity in a mouse model of Alzheimer’s disease and reversal by mGluR5 modulator
Mandino F, Shen X, Desrosiers-Grégoire G, O’Connor D, Mukherjee B, Owens A, Qu A, Onofrey J, Papademetris X, Chakravarty M, Strittmatter S, Lake E. Aging-dependent loss of functional connectivity in a mouse model of Alzheimer’s disease and reversal by mGluR5 modulator. Molecular Psychiatry 2024, 30: 1730-1745. PMID: 39424929, PMCID: PMC12015114, DOI: 10.1038/s41380-024-02779-z.Peer-Reviewed Original ResearchFunctional connectivity deficitsConnectivity deficitsFunctional connectivityBrain connectivityAllosteric modulators of mGluR5Alzheimer's diseaseDefault-mode networkModulation of mGluR5Loss of functional connectivityResting-state fMRIApplication of fMRIWild-type controlsAged AD miceMouse model of Alzheimer's diseaseAD-related changesAD miceModel of Alzheimer's diseaseAssociated with synaptic damageMGluR5 modulationMonths of ageFMRI measurementsAmyloid accumulationDecreased connectivityBrain networksSilent allosteric modulatorsSingle‐Cell Patch‐Clamp/Proteomics of Human Alzheimer's Disease iPSC‐Derived Excitatory Neurons Versus Isogenic Wild‐Type Controls Suggests Novel Causation and Therapeutic Targets
Ghatak S, Diedrich J, Talantova M, Bhadra N, Scott H, Sharma M, Albertolle M, Schork N, Yates J, Lipton S. Single‐Cell Patch‐Clamp/Proteomics of Human Alzheimer's Disease iPSC‐Derived Excitatory Neurons Versus Isogenic Wild‐Type Controls Suggests Novel Causation and Therapeutic Targets. Advanced Science 2024, 11: e2400545. PMID: 38773714, PMCID: PMC11304297, DOI: 10.1002/advs.202400545.Peer-Reviewed Original ResearchAbundance of individual proteinsIsogenic wild-type controlsSingle-cell (scHuman AD brainsWild-type controlsSingle-cellAlzheimer's diseaseMulticellular organismsSingle-cell physiologyAD brainTherapeutic targetIndividual proteinsProteomic informationGenetic mutationsProteinProteomicsProtein expressionHiPSC-neuronsExcitatory neuronsElectrophysiological statusDisease statesPhysiologyElectrophysiological dataNeuronsNeuronal level
2023
The correlation of ESR1 genetic aberrations with estrogen receptor and progesterone receptor status in metastatic and primary estrogen receptor-positive breast carcinomas
Moreira-Dinzey J, Zhan H, Rozenblit M, Krishnamurti U, Harigopal M, Zhong M, Liang Y. The correlation of ESR1 genetic aberrations with estrogen receptor and progesterone receptor status in metastatic and primary estrogen receptor-positive breast carcinomas. Human Pathology 2023, 137: 56-62. PMID: 37127079, DOI: 10.1016/j.humpath.2023.04.017.Peer-Reviewed Original ResearchConceptsMetastatic tumorsBreast carcinomaGenetic aberrationsPR statusPrimary tumorBreast cancerControl groupER/PR statusEstrogen receptor-positive breast carcinomasER-positive breast cancerER positivity rateMetastatic breast cancerProgesterone receptor statusMetastatic breast carcinomaMore liver metastasesPrimary breast carcinomaWild-type groupEstrogen receptor 1 geneReceptor 1 geneWild-type controlsLiver metastasesReceptor statusClinicopathological featuresER expressionControl tumors
2022
Loss of chaperone-mediated autophagy is associated with low vertebral cancellous bone mass
Akel N, MacLeod R, Berryhill S, Laster D, Dimori M, Crawford J, Fu Q, Onal M. Loss of chaperone-mediated autophagy is associated with low vertebral cancellous bone mass. Scientific Reports 2022, 12: 3134. PMID: 35210514, PMCID: PMC8873216, DOI: 10.1038/s41598-022-07157-9.Peer-Reviewed Original ResearchConceptsProtein degradation pathwaysRole of CMACRISPR-Cas9-based genome editingChaperone-mediated autophagySkeletal homeostasisDegradation pathwayProteome remodelingMouse genomeGene trapCytoplasmic proteinsOsteoblastic cell lineGenome editingProteasomal degradationSpecific knockdownWild-type controlsCell typesLAMP2ACultured cellsOsteoblast formationCell linesRANKL expressionCathepsin K.Pathophysiological conditionsAutophagyCMA processIntra-amniotic Injection of Poly(lactic-co-glycolic Acid) Microparticles Loaded with Growth Factor: Effect on Tissue Coverage and Cellular Apoptosis in the Rat Model of Myelomeningocele.
Maassel NL, Wu DH, Yung NK, Bauer-Pisani T, Elizabeth Guerra M, Ullrich SJ, Mark Saltzman W, Stitelman DH. Intra-amniotic Injection of Poly(lactic-co-glycolic Acid) Microparticles Loaded with Growth Factor: Effect on Tissue Coverage and Cellular Apoptosis in the Rat Model of Myelomeningocele. Journal Of The American College Of Surgeons 2022, 234: 1010-1019. PMID: 35703790, DOI: 10.1097/xcs.0000000000000156.Peer-Reviewed Original ResearchConceptsSoft tissue coverageIntra-amniotic injectionFibroblast growth factorTissue coverageRat modelMMC defectsGrowth factorCellular apoptosisGestational day 17Spinal cord cellsSitu cell deathCell deathWild-type controlsHistologic evidenceTreatment optionsLifelong morbidityUtero treatmentNeurologic disordersRat damsCord cellsMyelomeningoceleDay 17Invasive platformIncidenceInjection
2020
Quantification of SV2A Binding in Rodent Brain Using [18F]SynVesT-1 and PET Imaging
Sadasivam P, Fang XT, Toyonaga T, Lee S, Xu Y, Zheng MQ, Spurrier J, Huang Y, Strittmatter SM, Carson RE, Cai Z. Quantification of SV2A Binding in Rodent Brain Using [18F]SynVesT-1 and PET Imaging. Molecular Imaging And Biology 2020, 23: 372-381. PMID: 33258040, PMCID: PMC8105262, DOI: 10.1007/s11307-020-01567-9.Peer-Reviewed Original ResearchConceptsBrain stemAlzheimer's diseaseMin postinjectionAnimal modelsAPP/PS1 miceReference regionStandardized uptake value ratioDynamic PET imaging dataUptake value ratioRodent brain tissueStatic PET scansDifferent imaging windowsPET imaging dataWild-type controlsReference tissue modelPS1 miceAD pathogenesisTherapeutic effectMouse modelRodent modelsLittermate controlsPET scansRodent brainPreclinical imaging studiesTherapeutic drug efficacyGene-environment interaction promotes Alzheimer's risk as revealed by synergy of repeated mild traumatic brain injury and mouse App knock-in
Chiasseu M, Fesharaki-Zadeh A, Saito T, Saido TC, Strittmatter SM. Gene-environment interaction promotes Alzheimer's risk as revealed by synergy of repeated mild traumatic brain injury and mouse App knock-in. Neurobiology Of Disease 2020, 145: 105059. PMID: 32858147, PMCID: PMC7572902, DOI: 10.1016/j.nbd.2020.105059.Peer-Reviewed Original ResearchConceptsMild traumatic brain injuryTraumatic brain injuryAlzheimer's diseaseBrain injuryGene-environment interactionsMild closed head injuryMorris water maze testAge-matched wild-type controlsStrong unmet needAccumulation of amyloidAge-matched miceClosed head injuryWater maze testNovel object recognitionPersistent cognitive deficitsProtein gene mutationsIba1 expressionWild-type controlsPhospho-tauClinical manifestationsAD pathologyAD symptomsHead injuryAD pathogenesisRisk factorsControl of Murine Primordial Follicle Growth Activation by IκB/NFκB Signaling
Wright CJ, Cari EL, Sandoval J, Bales E, Sam PK, Zarate MA, Polotsky AJ, Kallen AN, Johnson J. Control of Murine Primordial Follicle Growth Activation by IκB/NFκB Signaling. Reproductive Sciences 2020, 27: 2063-2074. PMID: 32542534, PMCID: PMC7529825, DOI: 10.1007/s43032-020-00225-3.Peer-Reviewed Original ResearchConceptsPrimordial follicle growth activationLargest human genome-wide association studyGrowth activationHuman genome-wide association studiesGenome-wide association studiesLigand/receptor interactionsTranscription factor NFκBInhibitory protein IκBαAssociation studiesIκB proteinsWild-type controlsInhibitory proteinProtein IκBαPrimordial stageNFκB signalingMechanistic insightsReceptor interactionProteinMurine ovariesNFκB pathwayKey membersNFκBSubunit p65NFκB activationIκBβ
2018
Knockout of alpha 5 nicotinic acetylcholine receptors subunit alters ethanol-mediated behavioral effects and reward in mice
Dawson A, Wolstenholme JT, Roni MA, Campbell VC, Jackson A, Slater C, Bagdas D, Perez EE, Bettinger JC, De Biasi M, Miles MF, Damaj MI. Knockout of alpha 5 nicotinic acetylcholine receptors subunit alters ethanol-mediated behavioral effects and reward in mice. Neuropharmacology 2018, 138: 341-348. PMID: 29944862, PMCID: PMC6400055, DOI: 10.1016/j.neuropharm.2018.06.031.Peer-Reviewed Original ResearchConceptsΑ5 nAChREthanol consumptionΑ5 nicotinic acetylcholine receptor (nAChR) subunitsAlcohol dependenceBehavioral effectsImportance of nAChRsΑ5 nAChR subunitΑ5-KO miceNicotinic acetylcholine receptor subunitsEthanol-induced hypothermiaAnxiolytic-like responseEthanol drinking behaviorVoluntary ethanol consumptionNicotinic acetylcholine receptorsΑ5 knockout miceAcetylcholine receptor subunitsTwo-bottle choiceDecreases ethanol intakePlace preference assayEthanol-induced behaviorsWild-type controlsKO miceRestraint stressDID paradigmEthanol intake
2017
Bidirectional Regulation of Aggression in Mice by Hippocampal Alpha-7 Nicotinic Acetylcholine Receptors
Lewis AS, Pittenger ST, Mineur YS, Stout D, Smith PH, Picciotto MR. Bidirectional Regulation of Aggression in Mice by Hippocampal Alpha-7 Nicotinic Acetylcholine Receptors. Neuropsychopharmacology 2017, 43: 1267-1275. PMID: 29114104, PMCID: PMC5916354, DOI: 10.1038/npp.2017.276.Peer-Reviewed Original ResearchConceptsΑ7 nAChRsDentate gyrusNicotinic acetylcholine receptorsGTS-21Resident-intruder interactionsAlpha 7 nicotinic acetylcholine receptorAcetylcholine receptorsΑ7 nicotinic acetylcholine receptorExcitatory-inhibitory balancePromising therapeutic interventionGranule cell activityAggressive behaviorResident-intruder testHippocampal α7Wild-type controlsUnderlying neurobiological substratesGABAergic interneuronsMale micePotential neural circuitsRegulation of aggressionGranule cellsTherapeutic interventionsPartial agonistBrain regionsCell activityFunctional Analysis Reveals Geographical Variation in Inhibitory Immune Responses Against a Polymorphic Malaria Antigen
Bei AK, Ahouidi AD, Dvorin JD, Miura K, Diouf A, Ndiaye D, Premji Z, Diakite M, Mboup S, Long CA, Duraisingh MT. Functional Analysis Reveals Geographical Variation in Inhibitory Immune Responses Against a Polymorphic Malaria Antigen. The Journal Of Infectious Diseases 2017, 216: 267-275. PMID: 28605544, PMCID: PMC5853457, DOI: 10.1093/infdis/jix280.Peer-Reviewed Original ResearchConceptsInhibitory immune responsesVaccine candidate antigenImmune responseTransgenic parasite linesMalaria-endemic regionsReticulocyte-binding protein homologuesMalaria vaccine candidateParasite linesWild-type controlsTotal IgGHumoral responseMalaria antigensAntibody responseVaccine candidatesCandidate antigensMalaria endemicityGrowth inhibition assaysInvasion ligandsAntigenic specificityImmunogenic domainsSpecific antibodiesEndemic sitesAntigenStandardized toolsInhibition assaysComparison of 10 murine models reveals a distinct biomechanical phenotype in thoracic aortic aneurysms
Bellini C, Bersi MR, Caulk AW, Ferruzzi J, Milewicz DM, Ramirez F, Rifkin DB, Tellides G, Yanagisawa H, Humphrey JD. Comparison of 10 murine models reveals a distinct biomechanical phenotype in thoracic aortic aneurysms. Journal Of The Royal Society Interface 2017, 14: 20161036. PMID: 28490606, PMCID: PMC5454287, DOI: 10.1098/rsif.2016.1036.Peer-Reviewed Original ResearchConceptsGenetic mutationsExtracellular matrix proteinsTransmembrane receptorsCytoskeletal proteinsMatrix proteinsWild-type controlsBiomechanical phenotypeDysfunctional mechanosensingExtracellular matrixDiverse mouse modelsSmooth muscle cellsMutationsMuscle cellsProteinAorta of miceMurine modelCellsMechanosensingElastic fiber integrityMouse modelMechanoregulationStructural integrityPhenotypeIntracellularIntegrityNOD2 deficiency exacerbates imiquimod-induced, psoriasis-like dermatitis
Singh T, Cipolla E, Singh S, Farber J. NOD2 deficiency exacerbates imiquimod-induced, psoriasis-like dermatitis. The Journal Of Immunology 2017, 198: 75.17-75.17. DOI: 10.4049/jimmunol.198.supp.75.17.Peer-Reviewed Original ResearchNucleotide-Binding Oligomerization DomainNod2-/- micePsoriasis-like dermatitisToll-like receptorsIL-22Levels of mRNAPattern recognition proteinsIL-17AUp-regulation of NOD2Inhibition of Toll-like receptorImiquimod-treated skinRecognition proteinsDecreased levels of mRNAOligomerization domainAutoimmune skin diseaseIncreased levels of mRNAWild-type controlsExpression of mRNAInactivating mutationsAntibacterial defenseImiquimod-inducedNOD2 deficiencyNOD2 functionT cellsIL-1ra
2016
TLR8 Couples SOCS-1 and Restrains TLR7-Mediated Antiviral Immunity, Exacerbating West Nile Virus Infection in Mice
Paul AM, Acharya D, Le L, Wang P, Stokic DS, Leis AA, Alexopoulou L, Town T, Flavell RA, Fikrig E, Bai F. TLR8 Couples SOCS-1 and Restrains TLR7-Mediated Antiviral Immunity, Exacerbating West Nile Virus Infection in Mice. The Journal Of Immunology 2016, 197: 4425-4435. PMID: 27798161, PMCID: PMC5123688, DOI: 10.4049/jimmunol.1600902.Peer-Reviewed Original ResearchConceptsWest Nile virusAntiviral immunityWNV infectionWest Nile virus infectionOverexpression of TLR7Induced IFNsWild-type controlsSuppressor of cytokineTLR7 expressionNeuronal deathVirus infectionHuman TLR7TLR7TLR8InfectionMiceX proteinReduced expressionImmunityNile virusSOCS-1RNA knockdownIFNNovel roleProapoptotic genes
2015
Acetylation of TUG Protein Promotes the Accumulation of GLUT4 Glucose Transporters in an Insulin-responsive Intracellular Compartment*
Belman JP, Bian RR, Habtemichael EN, Li DT, Jurczak MJ, Alcázar-Román A, McNally LJ, Shulman GI, Bogan JS. Acetylation of TUG Protein Promotes the Accumulation of GLUT4 Glucose Transporters in an Insulin-responsive Intracellular Compartment*. Journal Of Biological Chemistry 2015, 290: 4447-4463. PMID: 25561724, PMCID: PMC4326849, DOI: 10.1074/jbc.m114.603977.Peer-Reviewed Original ResearchMeSH Keywords3T3-L1 CellsAcetylationAdipocytesAnimalsBlotting, WesternCarrier ProteinsCell MembraneCells, CulturedCystinyl AminopeptidaseCytoplasmFlow CytometryGlucoseGlucose Transporter Type 4HumansHypoglycemic AgentsImmunoprecipitationInsulinIntracellular Signaling Peptides and ProteinsMaleMiceMice, Inbred C57BLMice, KnockoutProtein TransportReal-Time Polymerase Chain ReactionReverse Transcriptase Polymerase Chain ReactionRNA, MessengerSirtuin 2ConceptsGLUT4 storage vesiclesGLUT4 glucose transportersInsulin-regulated aminopeptidaseGolgin-160Acetylated residuesC-terminusGolgi matrix proteinsSirtuin 2Insulin-responsive vesiclesGlucose transporterUnstimulated cellsGLUT4 traffickingInsulin-stimulated glucose uptakeGlucose uptakeC-terminal peptidePlasma membraneIntracellular compartmentsMatrix proteinsACBD3Protein promotesWild-type controlsDependent deacetylaseGLUT4Proteolytic processingIntracellular retention
2014
Hypothalamic prolyl endopeptidase (PREP) regulates pancreatic insulin and glucagon secretion in mice
Kim JD, Toda C, D’Agostino G, Zeiss CJ, DiLeone RJ, Elsworth JD, Kibbey RG, Chan O, Harvey BK, Richie CT, Savolainen M, Myöhänen T, Jeong JK, Diano S. Hypothalamic prolyl endopeptidase (PREP) regulates pancreatic insulin and glucagon secretion in mice. Proceedings Of The National Academy Of Sciences Of The United States Of America 2014, 111: 11876-11881. PMID: 25071172, PMCID: PMC4136568, DOI: 10.1073/pnas.1406000111.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBlood GlucoseGene ExpressionGene Knockdown TechniquesGlucagonGlucose Clamp TechniqueGlucose IntoleranceHypothalamusIndolesInsulinInsulin SecretionIon ChannelsMaleMiceMice, TransgenicMitochondrial ProteinsPancreasPhosphorylationProlyl OligopeptidasesReceptor, InsulinRecombinant ProteinsSerine EndopeptidasesSerine Proteinase InhibitorsThiazolidinesUncoupling Protein 1Ventromedial Hypothalamic NucleusConceptsWild-type miceGlucose intoleranceGlucagon secretionProlyl endopeptidaseHyperinsulinemic-euglycemic clamp studiesWild-type control miceGlucose-induced insulin releaseGlucose-induced insulin secretionEuglycemic clamp studiesAutonomic nervous systemVMH injectionsSympathetic outflowWild-type controlsNorepinephrine levelsGlucagon levelsGlucose toleranceControl miceInsulin levelsCentral infusionPancreatic functionVentromedial nucleusInsulin secretionNeuronal activationGlucose-intolerant phenotypeCentral regulationMacrophage migration inhibitory factor deficiency in chronic obstructive pulmonary disease
Sauler M, Leng L, Trentalange M, Haslip M, Shan P, Piecychna M, Zhang Y, Andrews N, Mannam P, Allore H, Fried T, Bucala R, Lee PJ. Macrophage migration inhibitory factor deficiency in chronic obstructive pulmonary disease. American Journal Of Physiology - Lung Cellular And Molecular Physiology 2014, 306: l487-l496. PMID: 24441872, PMCID: PMC3949087, DOI: 10.1152/ajplung.00284.2013.Peer-Reviewed Original ResearchMeSH KeywordsAdolescentAdultAge FactorsAgedAged, 80 and overAnimalsApoptosisCellular SenescenceCyclin-Dependent Kinase Inhibitor p16Cyclin-Dependent Kinase Inhibitor p21EmphysemaFemaleHumansIntramolecular OxidoreductasesLungMacrophage Migration-Inhibitory FactorsMaleMiceMice, Inbred C57BLMice, KnockoutMiddle AgedNicotianaPulmonary Disease, Chronic ObstructiveReceptors, ImmunologicSmokeSmokingTumor Suppressor Protein p53Young AdultConceptsChronic obstructive pulmonary diseaseMacrophage migration inhibitory factorPathogenesis of COPDDevelopment of COPDMIF receptor CD74Obstructive pulmonary diseasePulmonary diseaseWT miceReceptor CD74Role of MIFMacrophage migration inhibitory factor deficiencyMigration inhibitory factorNormal alveolar structureMo of ageWild-type controlsMIF concentrationsFormer smokersLung volumePlasma concentrationsSpontaneous emphysemaFactor deficiencyCigarette smokePleiotropic cytokineInhibitory factorAlveolar structures
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