2023
TMEM106B Puncta Is Increased in Multiple Sclerosis Plaques, and Reduced Protein in Mice Results in Delayed Lipid Clearance Following CNS Injury
Shafit-Zagardo B, Sidoli S, Goldman J, DuBois J, Corboy J, Strittmatter S, Guzik H, Edema U, Arackal A, Botbol Y, Merheb E, Nagra R, Graff S. TMEM106B Puncta Is Increased in Multiple Sclerosis Plaques, and Reduced Protein in Mice Results in Delayed Lipid Clearance Following CNS Injury. Cells 2023, 12: 1734. PMID: 37443768, PMCID: PMC10340176, DOI: 10.3390/cells12131734.Peer-Reviewed Original ResearchConceptsAxonal damageMultiple sclerosisRelapsing-remitting multiple sclerosisHypomorphic miceExperimental autoimmune encephalomyelitisRelapsing-remitting MSNormal-appearing white matterMultiple sclerosis plaquesWhite matter plaquesNon-neurologic controlsWild-type miceBrains of individualsLipid droplet accumulationAutoimmune encephalomyelitisMyelin oligodendrocyteCNS injuryLipid clearanceSpinal cordNeuronal integrityTransmembrane protein 106BWhite matterAlzheimer's diseaseMice resultsDroplet accumulationPlaques
2022
Endothelial Cell-Pericyte Interactions in the Pathogenesis of Cerebral Cavernous Malformations (CCMs).
Min W, Zhou JH. Endothelial Cell-Pericyte Interactions in the Pathogenesis of Cerebral Cavernous Malformations (CCMs). Cold Spring Harbor Perspectives In Medicine 2022, 13: a041188. PMID: 35667709, PMCID: PMC9760308, DOI: 10.1101/cshperspect.a041188.Peer-Reviewed Original ResearchConceptsCerebral cavernous malformationsCCM lesionsEndothelial cellsCavernous malformationsEndothelial cell-pericyte interactionsEC-specific deletionBrain vasculatureMice resultsLesion formationParenchymal cellsCCM formationLesionsPericytesPrimary defectFunction mutationsMalformationsUnexpected findingCell typesUbiquitous expressionCellsPatients
2021
Selective Overexpression of Collybistin in Mouse Hippocampal Pyramidal Cells Enhances GABAergic Neurotransmission and Protects against PTZ-Induced Seizures
George S, James S, De Blas A. Selective Overexpression of Collybistin in Mouse Hippocampal Pyramidal Cells Enhances GABAergic Neurotransmission and Protects against PTZ-Induced Seizures. ENeuro 2021, 8: eneuro.0561-20.2021. PMID: 34083383, PMCID: PMC8281261, DOI: 10.1523/eneuro.0561-20.2021.Peer-Reviewed Original ResearchConceptsHippocampal pyramidal cellsPyramidal cellsPyramidal neuronsAdeno-associated virusGABAergic synaptic transmissionCortical pyramidal neuronsHippocampal pyramidal neuronsMouse hippocampal pyramidal cellsCultured hippocampal neuronsAbsence of gephyrinCre-dependent mannerGABAergic neurotransmissionCre miceInhibitory neurotransmissionHippocampal interneuronsInhibitory postsynapsesInhibitory synapsesHippocampal neuronsSynaptic transmissionTarget neuronsPostsynaptic sitesBrain regionsMice resultsSelective overexpressionGlycinergic postsynapsesGIMAP5 maintains liver endothelial cell homeostasis and prevents portal hypertension
Drzewiecki K, Choi J, Brancale J, Leney-Greene MA, Sari S, Dalgiç B, Aksu A, Şahin G, Ozen A, Baris S, Karakoc-Aydiner E, Jain D, Kleiner D, Schmalz M, Radhakrishnan K, Zhang J, Hoebe K, Su HC, Pereira JP, Lenardo MJ, Lifton RP, Vilarinho S. GIMAP5 maintains liver endothelial cell homeostasis and prevents portal hypertension. Journal Of Experimental Medicine 2021, 218: e20201745. PMID: 33956074, PMCID: PMC8105721, DOI: 10.1084/jem.20201745.Peer-Reviewed Original ResearchConceptsLiver sinusoidal endothelial cellsPortal hypertensionEndothelial cell homeostasisHepatic endothelial cellsEndothelial cellsLiver diseaseUnexplained portal hypertensionGlobal health problemSinusoidal endothelial cellsCell homeostasisSingle-cell RNA-sequencing analysisHypertensionMouse modelHealth problemsMice resultsGimap5RNA sequence analysisMajor contributorCritical regulatorDiseaseCellsDamaging mutationsHomeostasisDecompensationMorbidity
2020
Mitochondrial Stress Response Gene Clpp Is Not Required for Granulosa Cell Function
Esencan E, Cozzolino M, Imamoglu G, Seli E. Mitochondrial Stress Response Gene Clpp Is Not Required for Granulosa Cell Function. Antioxidants 2020, 10: 1. PMID: 33374937, PMCID: PMC7821922, DOI: 10.3390/antiox10010001.Peer-Reviewed Original ResearchMitochondrial unfolded protein responseUnfolded mitochondrial proteinsLoss of ClpPGerminal vesicleUnfolded protein responseCell functionCumulus cell functionGranulosa/cumulus cellsMitochondrial proteinsClpP deletionClpPProtein responseGermline deletionMetabolic stressGranulosa cell functionDeletionUPRCumulus cellsMice resultsSimilar numberMII oocytesFemale miceWild-type miceEarly antralCells
2019
Translational activation of maternally derived mRNAs in oocytes and early embryos and the role of embryonic poly(A) binding protein (EPAB)
Esencan E, Kallen A, Zhang M, Seli E. Translational activation of maternally derived mRNAs in oocytes and early embryos and the role of embryonic poly(A) binding protein (EPAB). Biology Of Reproduction 2019, 100: 1147-1157. PMID: 30806655, PMCID: PMC8127035, DOI: 10.1093/biolre/ioz034.Peer-Reviewed Original ResearchConceptsTranslational activationBinding proteinSpecific protein complexesTranslation of mRNAsOocyte maturationCis-acting sequencesEarly embryo developmentProtein complexesXenopus modelEarly embryosKey regulatorGene expressionMolecular mechanismsEmbryo developmentTargeted disruptionMechanistic detailsProteinEarly developmentMRNAMice resultsKey mechanismOocytesActivationMaturationTranscription
2016
Kidney Tubular Ablation of Ocrl/Inpp5b Phenocopies Lowe Syndrome Tubulopathy
Inoue K, Balkin DM, Liu L, Nandez R, Wu Y, Tian X, Wang T, Nussbaum R, De Camilli P, Ishibe S. Kidney Tubular Ablation of Ocrl/Inpp5b Phenocopies Lowe Syndrome Tubulopathy. Journal Of The American Society Of Nephrology 2016, 28: 1399-1407. PMID: 27895154, PMCID: PMC5407733, DOI: 10.1681/asn.2016080913.Peer-Reviewed Original ResearchConceptsEarly embryonic lethalityTransporter 5Dent's diseaseIndependent endocytosisEmbryonic lethalityRedundant functionsType 2 inositolHuman phenotypesProximal tubule endocytosisOculocerebrorenal syndromeGenetic ablationCellular levelGermline knockoutLowe syndromeEndocytosisMouse backgroundMice resultsMutationsInositolLow molecular weight proteinuriaINPP5BParalogsProximal tubule functionDramatic effectOCRLSyndecan 4 controls lymphatic vasculature remodeling during mouse embryonic development
Wang Y, Baeyens N, Corti F, Tanaka K, Fang JS, Zhang J, Jin Y, Coon B, Hirschi KK, Schwartz MA, Simons M. Syndecan 4 controls lymphatic vasculature remodeling during mouse embryonic development. Development 2016, 143: 4441-4451. PMID: 27789626, PMCID: PMC5201046, DOI: 10.1242/dev.140129.Peer-Reviewed Original ResearchConceptsLymphatic endothelial cellsPlanar cell polarity protein Vangl2Lymphatic vessel remodelingMouse embryonic developmentHuman lymphatic endothelial cellsVangl2 overexpressionVangl2 expressionEmbryonic developmentValve morphogenesisEndothelial cellsVasculature developmentSyndecan-4Lymphatic vasculatureFluid shear stressSDC4Double knockout miceMice resultsHigh expressionVessel remodelingLymphatic vesselsExpressionVangl2RemodelingCellsMorphogenesis
2015
mTORC1 Activation Blocks Braf V600E -Induced Growth Arrest but Is Insufficient for Melanoma Formation
Damsky W, Micevic G, Meeth K, Muthusamy V, Curley DP, Santhanakrishnan M, Erdelyi I, Platt JT, Huang L, Theodosakis N, Zaidi MR, Tighe S, Davies MA, Dankort D, McMahon M, Merlino G, Bardeesy N, Bosenberg M. mTORC1 Activation Blocks Braf V600E -Induced Growth Arrest but Is Insufficient for Melanoma Formation. Cancer Cell 2015, 27: 41-56. PMID: 25584893, PMCID: PMC4295062, DOI: 10.1016/j.ccell.2014.11.014.Peer-Reviewed Original ResearchMeSH KeywordsAMP-Activated Protein KinasesAnimalsCell Line, TumorCell ProliferationCyclin-Dependent Kinase Inhibitor p16HumansMechanistic Target of Rapamycin Complex 1Mechanistic Target of Rapamycin Complex 2MelanocytesMelanoma, ExperimentalMiceMicroRNAsMolecular Sequence DataMultiprotein ComplexesMutationNevusProtein Serine-Threonine KinasesProto-Oncogene Proteins B-rafSignal TransductionSkin NeoplasmsTOR Serine-Threonine KinasesConceptsMelanoma formationGrowth arrestStable growth arrestMTORC2/AktSTK11 lossCDKN2A lossAkt activationIGF1R signalingMice resultsActivationArrestMTORC2Nevus developmentMTORC1/2SignalingAktMelanocytic nevus developmentMelanomagenesisMTORProgressionCDKN2AMelanocytesInactivationUpregulationComplete progression
2014
Hematopoietic Akt2 deficiency attenuates the progression of atherosclerosis
Rodlan N, Chamorro‐Jorganes A, Araldi E, Wanschel AC, Aryal B, Aranda JF, Goedeke L, Salerno AG, Ramírez CM, Sessa WC, Suárez Y, Fernández‐Hernando C. Hematopoietic Akt2 deficiency attenuates the progression of atherosclerosis. The FASEB Journal 2014, 29: 597-610. PMID: 25392271, PMCID: PMC4314230, DOI: 10.1096/fj.14-262097.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAtherosclerosisBlood GlucoseBone Marrow CellsBone Marrow TransplantationCell MovementCholesterolCytokinesDisease ProgressionInflammationInsulinLeukocytesLipidsLipoproteins, LDLMacrophagesMaleMiceMice, Inbred C57BLMice, KnockoutMicroscopy, ConfocalMicroscopy, FluorescencePlaque, AtheroscleroticProto-Oncogene Proteins c-aktReceptors, LDLConceptsProgression of atherosclerosisSerine-threonine protein kinaseBone marrow cellsAkt2-deficient miceInsulin-responsive tissuesWild-type bone marrow cellsProtein kinaseMarrow cellsAkt2 deficiencyAkt2Higher plasma lipidsWild-type miceMice resultsProatherogenic cytokinesObese subjectsPlasma lipidsProinflammatory cytokinesInsulin resistanceInflammatory responseGlucose levelsAtherosclerotic plaquesCholesterol metabolismAtherosclerosisMacrophage migrationMarked reductionTolerance to Acetaminophen Hepatotoxicity in the Mouse Model of Autoprotection Is Associated with Induction of Flavin-Containing Monooxygenase-3 (FMO3) in Hepatocytes
Rudraiah S, Rohrer P, Gurevich I, Goedken M, Rasmussen T, Hines R, Manautou J. Tolerance to Acetaminophen Hepatotoxicity in the Mouse Model of Autoprotection Is Associated with Induction of Flavin-Containing Monooxygenase-3 (FMO3) in Hepatocytes. Toxicological Sciences 2014, 141: 263-277. PMID: 24973094, PMCID: PMC4271123, DOI: 10.1093/toxsci/kfu124.Peer-Reviewed Original ResearchConceptsMale C57BL/6J miceAPAP hepatotoxicityFlavin-Containing Monooxygenase 3Protein expressionC57BL/6J miceFemale miceMouse modelMRNA levelsFirst time inductionNovel protective functionSingle doseAPAP treatmentMale miceAPAP cytotoxicityAcetaminophen pretreatmentHepatotoxic doseHigh doseAcetaminophen hepatotoxicityHepatotoxicityMice resultsCell line clonesMRNA expressionFMO3 expressionMiceAPAPLoss of Cbl–PI3K interaction in mice prevents significant bone loss following ovariectomy
Adapala NS, Holland D, Scanlon V, Barbe MF, Langdon WY, Tsygankov AY, Lorenzo JA, Sanjay A. Loss of Cbl–PI3K interaction in mice prevents significant bone loss following ovariectomy. Bone 2014, 67: 1-9. PMID: 24994594, PMCID: PMC4149851, DOI: 10.1016/j.bone.2014.06.013.Peer-Reviewed Original ResearchConceptsCbl-PI3K interactionSignificant bone lossBone lossSerum levelsBone resorptionBone remodelingPro-collagen type 1Bone resorbing activityDefective bone resorptionC-terminal telopeptideP1NP levelsSerum CTXResorbing activityL2 vertebraBone volumeOvariectomyTyrosine 737Mice resultsType 1Lumbar vertebraeMiceBone formationOsteoclast migrationBone developmentResorption
2013
Alterations in Glucose Homeostasis in a Murine Model of Chagas Disease
Nagajyothi F, Kuliawat R, Kusminski CM, Machado FS, Desruisseaux MS, Zhao D, Schwartz GJ, Huang H, Albanese C, Lisanti MP, Singh R, Li F, Weiss LM, Factor SM, Pessin JE, Scherer PE, Tanowitz HB. Alterations in Glucose Homeostasis in a Murine Model of Chagas Disease. American Journal Of Pathology 2013, 182: 886-894. PMID: 23321322, PMCID: PMC3586686, DOI: 10.1016/j.ajpath.2012.11.027.Peer-Reviewed Original ResearchConceptsPancreatic β-cellsChagas diseaseΒ-cellsGlucose-6-phosphatase mRNAChronic phaseInsulin levelsCruzi infectionGlucose homeostasisPlasma membraneInsulin granulesΒ-cell dysfunctionTrypanosoma cruziHost glucose homeostasisT. cruzi infectionElevated glucagon levelsΑ-cell functionAdrenergic receptor agonistDiminished insulin responsePancreatic islet architectureReduced insulinMice resultsAcute infectionCardiac dysfunctionGlucagon levelsPancreatic inflammation
2012
An evolutionarily conserved mode of modulation of Shaw‐like K+ channels
Cotella D, Hernandez‐Enriquez B, Duan Z, Wu X, Gazula V, Brown MR, Kaczmarek LK, Sesti F. An evolutionarily conserved mode of modulation of Shaw‐like K+ channels. The FASEB Journal 2012, 27: 1381-1393. PMID: 23233530, PMCID: PMC3606535, DOI: 10.1096/fj.12-222778.Peer-Reviewed Original ResearchConceptsEffect of phosphorylationC. elegansACP-2Acid phosphataseMammalian homologMammalian homologueCaenorhabditis elegansMouse nervous systemRegulatory partnersBiochemical experimentsMolecular mechanismsElegansBehavioral defectsMode of modulationPhosphorylationPharmacological disruptionShaw familyMammalian brainSubset of neuronsVentricular zonePhosphataseModel systemNervous systemMice resultsElectrophysiological analysisFoxO1 Target Gpr17 Activates AgRP Neurons to Regulate Food Intake
Ren H, Orozco IJ, Su Y, Suyama S, Gutiérrez-Juárez R, Horvath TL, Wardlaw SL, Plum L, Arancio O, Accili D. FoxO1 Target Gpr17 Activates AgRP Neurons to Regulate Food Intake. Cell 2012, 149: 1314-1326. PMID: 22682251, PMCID: PMC3613436, DOI: 10.1016/j.cell.2012.04.032.Peer-Reviewed Original ResearchConceptsFood intakeAgRP neuronsG-protein-coupled receptor GPR17Intracerebroventricular injectionHypothalamic neuronsReceptor GPR17Pharmacological modulationGlucose homeostasisNutritional statusTherapeutic potentialMice resultsGenetic ablationNeuronsFoxO1 ablationIntakeSatietyGPR17InsulinExpression profilingAblationPathwayCangrelorObesityLeptinAgonistsDisease-drug pairs revealed by computational genomic connectivity mapping on GBA1 deficient, Gaucher disease mice
Yuen T, Iqbal J, Zhu LL, Sun L, Lin A, Zhao H, Liu J, Mistry PK, Zaidi M. Disease-drug pairs revealed by computational genomic connectivity mapping on GBA1 deficient, Gaucher disease mice. Biochemical And Biophysical Research Communications 2012, 422: 573-577. PMID: 22588172, PMCID: PMC3377787, DOI: 10.1016/j.bbrc.2012.05.027.Peer-Reviewed Original ResearchConceptsMacrophage-directed therapiesConnectivity mappingAutoimmune diathesisDisease miceImmune cellsNew agentsMice resultsLiver cellsGlucocerebrosidase geneDrug pairsInstitute databaseDisease phenotypeMiceDisease-drug pairsDiverse populationsCMAPCellsGammopathyDysfunctionTherapyDiathesisFuture testingAlbendazoleDiseaseCaveolae, Fenestrae and Transendothelial Channels Retain PV1 on the Surface of Endothelial Cells
Tkachenko E, Tse D, Sideleva O, Deharvengt SJ, Luciano MR, Xu Y, McGarry CL, Chidlow J, Pilch PF, Sessa WC, Toomre DK, Stan RV. Caveolae, Fenestrae and Transendothelial Channels Retain PV1 on the Surface of Endothelial Cells. PLOS ONE 2012, 7: e32655. PMID: 22403691, PMCID: PMC3293851, DOI: 10.1371/journal.pone.0032655.Peer-Reviewed Original ResearchConceptsFormation of diaphragmsRemoval of caveolaeDynamin-independent pathwayAbsence of caveolaeEndothelial cellsProtein levelsCellular rolesCavin-1Knockout phenotypesPlasma membraneCaveolin-1CaveolaeLung endothelial cellsCell surfaceRapid internalizationInternalization rateAbundance of structuresMice resultsTransendothelial channelsEssential componentOnly roleFenestral diaphragmsCellsClathrinTranscription
2010
MAL/VIP17, a New Player in the Regulation of NKCC2 in the Kidney
Carmosino M, Rizzo F, Procino G, Basco D, Valenti G, Forbush B, Schaeren-Wiemers N, Caplan MJ, Svelto M. MAL/VIP17, a New Player in the Regulation of NKCC2 in the Kidney. Molecular Biology Of The Cell 2010, 21: 3985-3997. PMID: 20861303, PMCID: PMC2982131, DOI: 10.1091/mbc.e10-05-0456.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBlotting, WesternCell LineEndocytosisEpithelial CellsHumansImmunoprecipitationKidneyLLC-PK1 CellsMembrane Transport ProteinsMiceMice, TransgenicMyelin and Lymphocyte-Associated Proteolipid ProteinsMyelin ProteinsPhosphorylationProtein BindingProteolipidsRatsRats, Inbred WKYRNA InterferenceSodium-Potassium-Chloride SymportersSolute Carrier Family 12, Member 1SwineConceptsRegulation of NKCC2Apical membraneMajor salt transport pathwayC-terminal tailCell surface retentionApical sortingPorcine kidney cellsCotransporter phosphorylationTransgenic mice resultsNephron structuresRegulated absorptionImportant roleNew playersKidney cellsSurface expressionMice resultsSurface retentionTransport pathwaysNKCC2MembraneRegulationLymphocyte-associated proteinCyst formationRat kidney medullaColocalize
2009
Cutting Edge: Limiting MHC Class II Expression to Dendritic Cells Alters the Ability to Develop Th2- Dependent Allergic Airway Inflammation
Niu N, Laufer T, Homer RJ, Cohn L. Cutting Edge: Limiting MHC Class II Expression to Dendritic Cells Alters the Ability to Develop Th2- Dependent Allergic Airway Inflammation. The Journal Of Immunology 2009, 183: 1523-1527. PMID: 19596982, DOI: 10.4049/jimmunol.0901349.Peer-Reviewed Original ResearchConceptsAllergic airway inflammationMHC class II expressionAirway inflammationDendritic cellsClass II expressionTh2 generationTh2 immunityTh2-dependent allergic airway inflammationTh1 immune responseIFN-gamma productionAirway neutrophiliaTh2 primingRespiratory tractTh2 cellsImmune responseClass II signalsInflammationTh2 recruitmentMice resultsMiceCells altersImmunityActivationCellsNeutrophilia
2008
Knockout of STriatal enriched protein tyrosine phosphatase in mice results in increased ERK1/2 phosphorylation
Venkitaramani DV, Paul S, Zhang Y, Kurup P, Ding L, Tressler L, Allen M, Sacca R, Picciotto MR, Lombroso PJ. Knockout of STriatal enriched protein tyrosine phosphatase in mice results in increased ERK1/2 phosphorylation. Synapse 2008, 63: 69-81. PMID: 18932218, PMCID: PMC2706508, DOI: 10.1002/syn.20608.Peer-Reviewed Original ResearchConceptsSTEP knockout miceStriatal enriched protein tyrosine phosphataseKnockout miceWild-type miceERK1/2 activityHomozygous knockout miceBrain-specific proteinsExtracellular signal-regulated kinase1/2Wild-type controlsCA2 regionKO miceSTEP protein levelsLateral nucleusCytoarchitectural abnormalitiesSynaptic stimulationCultured neuronsSynaptic plasticityMice resultsHeterozygous miceMiceERK1/2 phosphorylationProtein tyrosine phosphataseProtein levels
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