2023
Pathogenic RAB34 variants impair primary cilium assembly and cause a novel oral-facial-digital syndrome
Bruel A, Ganga A, Nosková L, Valenzuela I, Martinovic J, Duffourd Y, Zikánová M, Majer F, Kmoch S, Mohler M, Sun J, Sweeney L, Martínez-Gil N, Thauvin-Robinet C, Breslow D. Pathogenic RAB34 variants impair primary cilium assembly and cause a novel oral-facial-digital syndrome. Human Molecular Genetics 2023, 32: 2822-2831. PMID: 37384395, PMCID: PMC10481091, DOI: 10.1093/hmg/ddad109.Peer-Reviewed Original ResearchConceptsCilia assemblyCiliary membrane formationIntracellular ciliogenesis pathwayPrimary cilia assemblyBi-allelic missense variantsRab proteinsRab GTPaseCiliary proteinsSmall GTPaseNascent ciliaMother centriolePrimary ciliaC-terminusProtein productsPathogenic variantsRab34Cell typesFunctional impactMissense variantsGTPaseStrong lossCiliogenesisSignificant defectsGenesKey mediatorClinicoserological insights into patients with immune checkpoint inhibitor‐induced myasthenia gravis
Masi G, Pham M, Karatz T, Oh S, Payne A, Nowak R, Howard J, Guptill J, Juel V, O'Connor K. Clinicoserological insights into patients with immune checkpoint inhibitor‐induced myasthenia gravis. Annals Of Clinical And Translational Neurology 2023, 10: 825-831. PMID: 36924454, PMCID: PMC10187728, DOI: 10.1002/acn3.51761.Peer-Reviewed Original Research
2022
Tuft cells are key mediators of interkingdom interactions at mucosal barrier surfaces
Strine MS, Wilen CB. Tuft cells are key mediators of interkingdom interactions at mucosal barrier surfaces. PLOS Pathogens 2022, 18: e1010318. PMID: 35271673, PMCID: PMC8912186, DOI: 10.1371/journal.ppat.1010318.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsConceptsInterkingdom interactionsTuft cellsCell biologyImmune responseMicrobial activationMicrobial sensingCell abundanceMucosal barrier surfacesAntiviral adaptive immune responsesType 2 immune responsesCell heterogeneityExquisite specificityMucosal barrier integrityAdaptive immune responsesMurine norovirusHuman healthKey orchestratorsMicrobial infectionsPathogenic bacteriaBroad intraFlavivirus replicationKey mediatorContext of coinfectionTissue repairImmune evasion
2020
19. PLEKHA5 REGULATES TUMOR GROWTH IN METASTATIC MELANOMA
Oria V, Zhang H, Zhu H, Deng G, Zito C, Rane C, Zhang S, Weiss S, Tran T, Adeniran A, Zhang F, Zhou J, Kluger Y, Bosenberg M, Kluger H, Jilaveanu L. 19. PLEKHA5 REGULATES TUMOR GROWTH IN METASTATIC MELANOMA. Neuro-Oncology Advances 2020, 2: ii3-ii3. PMCID: PMC7401364, DOI: 10.1093/noajnl/vdaa073.009.Peer-Reviewed Original ResearchMelanoma brain metastasesBrain metastasesTumor growthPI3K/Akt/mTORCell cycle transitionAkt/mTORGrowth of tumorsS cell cycle transitionPhosphorylation of AktMelanoma patientsPoor prognosisNovel drug targetsPatient populationRegulation of PDCD4Metastatic melanomaUnique cohortXenograft modelClinical relevanceNude miceMetastasisCycle transitionMelanomaBrain developmentKey mediatorMelanoma cells
2019
O-GlcNAc transferase suppresses necroptosis and liver fibrosis
Zhang B, Li MD, Yin R, Liu Y, Yang Y, Mitchell-Richards KA, Nam JH, Li R, Wang L, Iwakiri Y, Chung D, Robert ME, Ehrlich BE, Bennett AM, Yu J, Nathanson MH, Yang X. O-GlcNAc transferase suppresses necroptosis and liver fibrosis. JCI Insight 2019, 4: e127709. PMID: 31672932, PMCID: PMC6948774, DOI: 10.1172/jci.insight.127709.Peer-Reviewed Original ResearchConceptsReceptor-interacting protein kinase 3Liver fibrosisLiver diseaseHepatocyte necroptosisEthanol-induced liver injuryAlcoholic liver cirrhosisChronic liver diseaseMultiple liver diseasesWeeks of ageProtein expression levelsPortal inflammationLiver cirrhosisLiver injuryBallooning degenerationElevated protein expression levelsSpontaneous genetic modelFibrosisKey suppressorKey mediatorMiceProtein kinase 3CirrhosisExpression levelsGlcNAc levelsMixed lineage kinaseNorovirus Attachment and Entry
Graziano VR, Wei J, Wilen CB. Norovirus Attachment and Entry. Viruses 2019, 11: 495. PMID: 31151248, PMCID: PMC6630345, DOI: 10.3390/v11060495.Peer-Reviewed Original ResearchConceptsHisto-blood group antigensNorovirus attachmentMajority of casesMajor human pathogenViral life cycleImmune interactionsViral gastroenteritisCell tropismGroup antigensViral entryKey mediatorHuman norovirusBile saltsViral genome releaseMurine norovirusReceptorsMinor capsid protein VP2Capsid protein VP2Human pathogensMolecular mechanismsNorovirusSignificant determinantsProtein VP2Important future directionsCurrent understandingA Further Analysis and Commentary on: Profiling Changes in Cortical Astroglial Cells Following Chronic Stress
Coppola G, Rurak GM, Simard S, Salmaso N. A Further Analysis and Commentary on: Profiling Changes in Cortical Astroglial Cells Following Chronic Stress. Neuroscience Insights 2019, 13: 1179069519870182. PMID: 31452604, PMCID: PMC6698990, DOI: 10.1177/1179069519870182.Peer-Reviewed Original ResearchGene co-expression network analysisCo-expression network analysisAnxiety-like behaviorKey transcription factorPerineuronal netsAstroglial cellsExtracellular matrix componentsTrophic pathwaysImportant extracellular matrix componentTranscription factorsProtein degradationChronic stressNeuroplasticity hypothesisKey regulatorExpression of PNNsNeural plasticityCortical astroglial cellsChronic variable stressTreatment of depressionMatrix componentsMajor depressive disorderProfiling changesCortical neural plasticityKey mediatorModulates neuroplasticity
2018
Acute physical exercise increases leptin‐induced hypothalamic extracellular signal‐regulated kinase1/2 phosphorylation and thermogenesis of obese mice
Gaspar R, Muñoz V, Kuga G, Nakandakari S, Minuzzi L, Botezelli J, da Silva A, Cintra D, de Moura L, Ropelle E, Pauli J. Acute physical exercise increases leptin‐induced hypothalamic extracellular signal‐regulated kinase1/2 phosphorylation and thermogenesis of obese mice. Journal Of Cellular Biochemistry 2018, 120: 697-704. PMID: 30206970, DOI: 10.1002/jcb.27426.Peer-Reviewed Original ResearchConceptsAcute physical exerciseBrown adipose tissueObese micePhysical exerciseEnergy expenditureERK1/2 phosphorylationTreatment of obesityExtracellular signal-regulated kinase1/2 (ERK1/2) phosphorylationProtein 1 (UCP1) contentExtracellular signal-regulated kinase 1/2Signal-regulated kinase 1/2Sympathetic signalsSpontaneous activityAdipose tissueP-ERK1/2Main interventionThermoregulatory effectsMiceKey mediatorThermogenesisOxygen uptakeMolecular changesKinase 1/2ObeseObesityPKCε contributes to lipid-induced insulin resistance through cross talk with p70S6K and through previously unknown regulators of insulin signaling
Gassaway BM, Petersen MC, Surovtseva YV, Barber KW, Sheetz JB, Aerni HR, Merkel JS, Samuel VT, Shulman GI, Rinehart J. PKCε contributes to lipid-induced insulin resistance through cross talk with p70S6K and through previously unknown regulators of insulin signaling. Proceedings Of The National Academy Of Sciences Of The United States Of America 2018, 115: e8996-e9005. PMID: 30181290, PMCID: PMC6156646, DOI: 10.1073/pnas.1804379115.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAnimals, Genetically ModifiedDiabetes Mellitus, Type 2Diet, High-FatDisease Models, AnimalGene Knockdown TechniquesHumansInsulinInsulin Receptor Substrate ProteinsInsulin ResistanceLipid MetabolismLiverPhosphorylationProtein Kinase C-epsilonProteomicsRatsReceptor, InsulinRibosomal Protein S6Ribosomal Protein S6 Kinases, 70-kDaRNA, Small InterferingSignal TransductionConceptsHigh-fat diet-induced hepatic insulin resistanceDiet-induced hepatic insulin resistanceLipid-induced insulin resistanceProtein phosphorylationSiRNA-based screenProtein kinase C εSet of proteinsCross talkHepatic insulin resistanceQuantitative phosphoproteomicsMotif analysisUnknown regulatorKinase assaysPhosphoproteomic dataCanonical insulinP70S6KInsulin receptorImpact of lipidSystem-level approachPKCεDiacylglycerolPhosphorylationKey mediatorNew therapeutic approachesInsulin resistanceToll-like receptor 4: a target for chemoprevention of hepatocellular carcinoma in obesity and steatohepatitis
Nguyen J, Jiao J, Smoot K, Watt G, Zhao C, Song X, Stevenson H, McCormick J, Fisher-Hoch S, Zhang J, Futreal P, Beretta L. Toll-like receptor 4: a target for chemoprevention of hepatocellular carcinoma in obesity and steatohepatitis. Oncotarget 2018, 9: 29495-29507. PMID: 30034633, PMCID: PMC6047684, DOI: 10.18632/oncotarget.25685.Peer-Reviewed Original ResearchNon-alcoholic fatty liver diseaseTLR4 mRNA expressionHepatocellular carcinomaMRNA expressionIL-6HCC patientsHCC developmentHCC tumorsIL-10 mRNA expressionToll-like receptor 4Fatty liver diseaseWhole-exome sequencingIngenuity Pathway AnalysisDistant liverIL-10Liver diseaseTLR4 inhibitorProinflammatory responseReceptor 4TLR4 activationHCC chemopreventionChemopreventionKey mediatorTumorsMiceProduction of BMP4 by endothelial cells is crucial for endogenous thymic regeneration
Wertheimer T, Velardi E, Tsai J, Cooper K, Xiao S, Kloss CC, Ottmüller KJ, Mokhtari Z, Brede C, deRoos P, Kinsella S, Palikuqi B, Ginsberg M, Young LF, Kreines F, Lieberman SR, Lazrak A, Guo P, Malard F, Smith OM, Shono Y, Jenq RR, Hanash AM, Nolan DJ, Butler JM, Beilhack A, Manley NR, Rafii S, Dudakov JA, van den Brink MRM. Production of BMP4 by endothelial cells is crucial for endogenous thymic regeneration. Science Immunology 2018, 3 PMID: 29330161, PMCID: PMC5795617, DOI: 10.1126/sciimmunol.aal2736.Peer-Reviewed Original ResearchConceptsKey transcription factorEndothelial cellsEndogenous tissue regenerationThymic epithelial cellsTranscription factorsBMP4 pathwayThymic endothelial cellsDownstream targetsBMP4Genetic inhibitionThymocyte developmentTEC developmentEpithelial cellsKey mediatorEndogenous regenerationRemarkable abilityCritical pathwaysTissue regenerationPathwayCellsRegenerationEndogenous thymic regenerationT cell immunityPotential clinical approachThymic damage
2017
Corticosteroid-induced dendrite loss and behavioral deficiencies can be blocked by activation of Abl2/Arg kinase
Shapiro LP, Omar MH, Koleske AJ, Gourley SL. Corticosteroid-induced dendrite loss and behavioral deficiencies can be blocked by activation of Abl2/Arg kinase. Molecular And Cellular Neuroscience 2017, 85: 226-234. PMID: 29107098, PMCID: PMC5767942, DOI: 10.1016/j.mcn.2017.10.007.Peer-Reviewed Original ResearchConceptsCorticosterone exposureHippocampal CA1 pyramidal neuronsStressor exposureArbor structureCA1 pyramidal neuronsAnhedonic-like behaviorClassical neurotransmitter systemsSpecific brain regionsMental health concernsDendrite lossPyramidal neuronsStress-related illnessesArg nonreceptor tyrosine kinaseNeuronal remodelingNeurotransmitter systemsNeural degenerationBehavioral abnormalitiesTrigger pointsCognitive declineBrain regionsKey next stepHealth concernKey mediatorMental healthPharmacological compoundsHave we pushed the needle for treatment of Type 1 diabetes?
Naushad N, Perdigoto AL, Rui J, Herold KC. Have we pushed the needle for treatment of Type 1 diabetes? Current Opinion In Immunology 2017, 49: 44-50. PMID: 28992525, PMCID: PMC5937133, DOI: 10.1016/j.coi.2017.09.004.Peer-Reviewed Original ResearchInduction of a BRCAness state by oncometabolites and exploitation by PARP inhibitors.
Bindra R, Sulkowski P, Corso C, Glazer P, Shuch B. Induction of a BRCAness state by oncometabolites and exploitation by PARP inhibitors. Journal Of Clinical Oncology 2017, 35: 11586-11586. DOI: 10.1200/jco.2017.35.15_suppl.11586.Peer-Reviewed Original ResearchAcute myeloid leukemiaMulti-center phase II trialIDH1/2 mutationsPARP inhibitorsMutant IDH1/2 inhibitorsPhase II trialEfficacy of olaparibPoly (ADP-ribose) polymerase (PARP) inhibitorsRelated gene mutationsHomologous recombination defectsII trialIDH1/2 inhibitorsMyeloid leukemiaIsocitrate dehydrogenase 1Therapeutic strategiesPathologic processesSmall molecule inhibitorsIDH1/2-mutant tumorsSmall molecule inhibitionTumor progressionDNA repair inhibitorsPolymerase inhibitorsModern oncologyTumor cellsKey mediator
2016
Large-scale mapping of gene regulatory logic reveals context-dependent repression by transcriptional activators
van Dijk D, Sharon E, Lotan-Pompan M, Weinberger A, Segal E, Carey LB. Large-scale mapping of gene regulatory logic reveals context-dependent repression by transcriptional activators. Genome Research 2016, 27: 87-94. PMID: 27965290, PMCID: PMC5204347, DOI: 10.1101/gr.212316.116.Peer-Reviewed Original ResearchConceptsTranscription factorsGene regulatory logicPromoter DNA sequencesGene expression outputActive transcription factorTarget gene expressionGene expression profilesMaximum promoter activityTranscriptional activatorExpression outputRegulatory logicDNA sequencesGene expressionPromoter activityIntracellular signalsExpression profilesTF moleculesActivity of thousandsActivator siteLocal poolAbsolute expressionTF concentrationPromoterKey mediatorExpressionMolecular Imaging of Angiogenesis and Vascular Remodeling in Cardiovascular Pathology
Golestani R, Jung JJ, Sadeghi MM. Molecular Imaging of Angiogenesis and Vascular Remodeling in Cardiovascular Pathology. Journal Of Clinical Medicine 2016, 5: 57. PMID: 27275836, PMCID: PMC4929412, DOI: 10.3390/jcm5060057.Peer-Reviewed Original ResearchVascular remodelingMolecular imaging techniquesPeripheral arterial diseaseSelection of patientsArt molecular imagingImaging techniquesVascular biology researchNuclear imaging techniquesMolecular imagingArterial diseaseRisk stratificationAortic aneurysmMyocardial ischemiaCardiovascular diseaseEarly diagnosisAnimal modelsCardiovascular pathologyTherapeutic interventionsCellular playersClinical toolKey mediatorAngiogenesisRemodelingClinical translationDiseaseMitochondrial Reactive Oxygen Species Mediate Cardiac Structural, Functional, and Mitochondrial Consequences of Diet‐Induced Metabolic Heart Disease
Sverdlov AL, Elezaby A, Qin F, Behring JB, Luptak I, Calamaras TD, Siwik DA, Miller EJ, Liesa M, Shirihai OS, Pimentel DR, Cohen RA, Bachschmid MM, Colucci WS. Mitochondrial Reactive Oxygen Species Mediate Cardiac Structural, Functional, and Mitochondrial Consequences of Diet‐Induced Metabolic Heart Disease. Journal Of The American Heart Association 2016, 5: e002555. PMID: 26755553, PMCID: PMC4859372, DOI: 10.1161/jaha.115.002555.Peer-Reviewed Original ResearchMeSH KeywordsAdenosine TriphosphateAnimalsCatalaseDiet, High-FatDietary SucroseDisease Models, AnimalElectron Transport Complex IElectron Transport Complex IIEnergy MetabolismHypertrophy, Left VentricularMice, Inbred C57BLMice, TransgenicMitochondria, HeartMitochondrial DiseasesMutationOxidation-ReductionOxidative StressProtein Processing, Post-TranslationalReactive Oxygen SpeciesVentricular Dysfunction, LeftVentricular Function, LeftConceptsOxidative posttranslational modificationsMitochondrial reactive oxygen speciesPosttranslational modificationsReactive oxygen speciesMetabolic heart diseaseATP synthesisMitochondrial dysfunctionCardiac mitochondrial proteinsSite-directed mutationsMitochondrial proteinsTransgenic miceWild-type miceComplex IMitochondriaMitochondrial abnormalitiesHigh palmitateOxygen speciesCardiac mitochondriaCys100Mitochondrial consequencesCys103Key mediatorProteinH2O2 productionHigh-fat high-sucrose diet
2015
IL-21 Promotes Pulmonary Fibrosis through the Induction of Profibrotic CD8+ T Cells
Brodeur TY, Robidoux TE, Weinstein JS, Craft J, Swain SL, Marshak-Rothstein A. IL-21 Promotes Pulmonary Fibrosis through the Induction of Profibrotic CD8+ T Cells. The Journal Of Immunology 2015, 195: 5251-5260. PMID: 26519529, PMCID: PMC4655158, DOI: 10.4049/jimmunol.1500777.Peer-Reviewed Original ResearchPhosphoinositide 3-Kinase-C2α Regulates Polycystin-2 Ciliary Entry and Protects against Kidney Cyst Formation
Franco I, Margaria JP, De Santis MC, Ranghino A, Monteyne D, Chiaravalli M, Pema M, Campa CC, Ratto E, Gulluni F, Perez-Morga D, Somlo S, Merlo GR, Boletta A, Hirsch E. Phosphoinositide 3-Kinase-C2α Regulates Polycystin-2 Ciliary Entry and Protects against Kidney Cyst Formation. Journal Of The American Society Of Nephrology 2015, 27: 1135-1144. PMID: 26271513, PMCID: PMC4814170, DOI: 10.1681/asn.2014100967.Peer-Reviewed Original ResearchConceptsPI3K-C2αCiliary componentsPolycystin-2Primary ciliaRecycling endosome compartmentKidney cyst formationDuct 3 cellsCiliary entryCilium baseElongation defectsCargo proteinsCilium morphogenesisSubcellular locationPhosphoinositide 3Endosome compartmentTubule developmentProliferation signalsCiliary transportCyst formationCystic kidney diseaseIschemia/reperfusion-induced renal damageGenetic modelsCiliaCyst developmentKey mediator
2013
CD301b+ Dermal Dendritic Cells Drive T Helper 2 Cell-Mediated Immunity
Kumamoto Y, Linehan M, Weinstein JS, Laidlaw BJ, Craft JE, Iwasaki A. CD301b+ Dermal Dendritic Cells Drive T Helper 2 Cell-Mediated Immunity. Immunity 2013, 39: 733-743. PMID: 24076051, PMCID: PMC3819035, DOI: 10.1016/j.immuni.2013.08.029.Peer-Reviewed Original ResearchConceptsDermal dendritic cellsDendritic cellsDermal DCsTh2 cellsT cellsT helper 2 cellsT helper responsesInterleukin-4 productionExpression of CD69Th2 cell developmentDC depletionLymph nodesTh2 immunityHelper responsesSubcutaneous immunizationNippostrongylus brasiliensisKey mediatorTransient depletionCell developmentImmunityOvalbuminDepletion approachCellsParticular subsetCD301b
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