2017
Disruptions in asymmetric centrosome inheritance and WDR62-Aurora kinase B interactions in primary microcephaly
Sgourdou P, Mishra-Gorur K, Saotome I, Henagariu O, Tuysuz B, Campos C, Ishigame K, Giannikou K, Quon JL, Sestan N, Caglayan AO, Gunel M, Louvi A. Disruptions in asymmetric centrosome inheritance and WDR62-Aurora kinase B interactions in primary microcephaly. Scientific Reports 2017, 7: 43708. PMID: 28272472, PMCID: PMC5341122, DOI: 10.1038/srep43708.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAurora Kinase BBrainCell CycleCell Cycle ProteinsCell DifferentiationCell ProliferationCentrosomeConsanguinityDisease Models, AnimalEpistasis, GeneticFluorescent Antibody TechniqueGene ExpressionHumansInheritance PatternsMaleMiceMice, KnockoutMicrocephalyMutationNerve Tissue ProteinsNeural Stem CellsPedigreeWhole Genome SequencingConceptsChromosome passenger complexPatient-derived fibroblastsCentrosome inheritanceNeocortical progenitorsDisease-associated mutant formsSpindle pole localizationAurora kinase BPassenger complexMitotic progressionMouse orthologDiverse functionsMutant formsWD repeat domain 62Key regulatorCPC componentsKinase BPole localizationPrimary microcephalyLate neurogenesisRecessive mutationsNeuronal differentiationWDR62Severe brain malformationsReduced proliferationNeocortical development
2016
Notch1 and Notch2 receptors regulate mouse and human gastric antral epithelial cell homoeostasis
Gifford GB, Demitrack ES, Keeley TM, Tam A, La Cunza N, Dedhia PH, Spence JR, Simeone DM, Saotome I, Louvi A, Siebel CW, Samuelson LC. Notch1 and Notch2 receptors regulate mouse and human gastric antral epithelial cell homoeostasis. Gut 2016, 66: 1001. PMID: 26933171, PMCID: PMC5009003, DOI: 10.1136/gutjnl-2015-310811.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntibodies, Monoclonal, HumanizedApoptosisCell DifferentiationCell ProliferationCells, CulturedDibenzazepinesEpithelial CellsFemaleGastric MucosaGene ExpressionHomeostasisHumansMaleMiceMice, Inbred C57BLMice, TransgenicOrganoidsPyloric AntrumReceptor, Notch1Receptor, Notch2Receptors, G-Protein-CoupledSignal TransductionStem CellsConceptsEpithelial cell homeostasisCell homeostasisNotch receptorsNotch inhibitor dibenzazepineGlobal Notch inhibitionStem cellsAntral stem cellsHuman antral glandsAnalysis of miceNotch pathway receptorsLgr5 stem cellsCellular differentiationNotch signalingNotch2 receptorMolecular approachesPathway receptorsNotch pathway inhibitionHuman organoidsEpithelial cell proliferationNotch inhibitionInhibition of Notch1Notch inhibitorsOrganoid growthCell proliferationNotch2
2014
Ccm3, a gene associated with cerebral cavernous malformations, is required for neuronal migration
Louvi A, Nishimura S, Günel M. Ccm3, a gene associated with cerebral cavernous malformations, is required for neuronal migration. Development 2014, 141: 1404-1415. PMID: 24595293, PMCID: PMC3943187, DOI: 10.1242/dev.093526.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApoptosis Regulatory ProteinsCell MovementCell ProliferationCyclin-Dependent Kinase 5FemaleHemangioma, Cavernous, Central Nervous SystemIntracellular Signaling Peptides and ProteinsMiceMice, KnockoutMice, TransgenicNeocortexNeural Stem CellsNeurogliaPregnancyRho GTP-Binding ProteinsRhoA GTP-Binding ProteinSignal TransductionConceptsCerebral cavernous malformation 3Neuronal migrationCerebral cavernous malformationsRadial glia progenitorsCell non-autonomous functionCerebrovascular disordersPyramidal neuronsCortical plateLaminar positioningSubventricular zoneCortical developmentCavernous malformationsRadial gliaLoss of functionNascent neuronsNeuronal morphologySevere malformationsGlia progenitorsNeural progenitorsNeuronsNon-autonomous functionsMalformationsRhoA pathwayPossible interactionsGlia
2011
Loss of cerebral cavernous malformation 3 (Ccm3) in neuroglia leads to CCM and vascular pathology
Louvi A, Chen L, Two AM, Zhang H, Min W, Günel M. Loss of cerebral cavernous malformation 3 (Ccm3) in neuroglia leads to CCM and vascular pathology. Proceedings Of The National Academy Of Sciences Of The United States Of America 2011, 108: 3737-3742. PMID: 21321212, PMCID: PMC3048113, DOI: 10.1073/pnas.1012617108.Peer-Reviewed Original ResearchConceptsNeural cellsCerebral cavernous malformationsCell-nonautonomous mechanismsPathogenesis of CCMsRho GTPase signalingCell-autonomous mechanismsCell-autonomous roleCerebral cavernous malformation 3Cell death 10Central nervous systemConditional mouse mutantsNonautonomous functionsCytoskeletal remodelingRNA sequencingCCM3/Mouse mutantsNeurovascular unitNonautonomous mechanismsProper developmentVascular lesionsGene 1Function mutationsNervous systemAutonomous mechanismsLate functions
2008
Cyst formation and activation of the extracellular regulated kinase pathway after kidney specific inactivation of Pkd1
Shibazaki S, Yu Z, Nishio S, Tian X, Thomson RB, Mitobe M, Louvi A, Velazquez H, Ishibe S, Cantley LG, Igarashi P, Somlo S. Cyst formation and activation of the extracellular regulated kinase pathway after kidney specific inactivation of Pkd1. Human Molecular Genetics 2008, 17: 1505-1516. PMID: 18263604, PMCID: PMC2902289, DOI: 10.1093/hmg/ddn039.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApoptosisButadienesCell ProliferationCystsDisease Models, AnimalEnzyme ActivationKidneyMAP Kinase Kinase 1MAP Kinase Kinase 2MiceMice, Mutant StrainsMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3NitrilesPolycystic Kidney, Autosomal DominantProtein Kinase InhibitorsTRPP Cation ChannelsConceptsCyst formationERK1/2 activationPostnatal day 21Renal cystic diseaseWeeks of birthCyst cell proliferationPolycystic kidney diseaseKinase pathwayKidney tubule cellsKidney-specific inactivationRenal failureMEK1/2 inhibitor U0126Kidney diseaseCystic diseaseMAPK/ERKMAPK/ERK activationPresence of ciliaProliferative indexCyst growthCyst expansionDay 21Tubule cellsBrdU uptakeCystic kidneysBromodeoxyuridine incorporation