2012
Altered subcellular localization of transcription factor TEAD4 regulates first mammalian cell lineage commitment
Home P, Saha B, Ray S, Dutta D, Gunewardena S, Yoo B, Pal A, Vivian JL, Larson M, Petroff M, Gallagher PG, Schulz VP, White KL, Golos TG, Behr B, Paul S. Altered subcellular localization of transcription factor TEAD4 regulates first mammalian cell lineage commitment. Proceedings Of The National Academy Of Sciences Of The United States Of America 2012, 109: 7362-7367. PMID: 22529382, PMCID: PMC3358889, DOI: 10.1073/pnas.1201595109.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBlastocystBlastocyst Inner Cell MassBlastomeresBlotting, WesternCattleCDX2 Transcription FactorCell LineageCell NucleusCells, CulturedDNA-Binding ProteinsEmbryonic Stem CellsGATA3 Transcription FactorGene Expression Regulation, DevelopmentalGreen Fluorescent ProteinsHEK293 CellsHomeodomain ProteinsHumansMacaca mulattaMiceMice, TransgenicMuscle ProteinsRatsReverse Transcriptase Polymerase Chain ReactionRNA InterferenceTEA Domain Transcription FactorsTranscription FactorsConceptsInner cell massTranscriptional programsICM lineagesSubcellular localizationNuclear localizationInner blastomeresCell fate specificationSpecific transcriptional programsCell lineage commitmentAltered subcellular localizationTranscription factor TEAD4Preimplantation mouse embryosFate specificationLineage commitmentTarget genesMouse embryosCell lineagesTEAD4LineagesBlastomeresBlastocyst formationCell massDifferential functionGenesLocalization
2011
Loss-of-function and gain-of-function phenotypes of stomatocytosis mutant RhAG F65S
Stewart AK, Shmukler BE, Vandorpe DH, Rivera A, Heneghan JF, Li X, Hsu A, Karpatkin M, O'Neill AF, Bauer DE, Heeney MM, John K, Kuypers FA, Gallagher PG, Lux SE, Brugnara C, Westhoff CM, Alper SL. Loss-of-function and gain-of-function phenotypes of stomatocytosis mutant RhAG F65S. American Journal Of Physiology - Cell Physiology 2011, 301: c1325-c1343. PMID: 21849667, PMCID: PMC3233792, DOI: 10.1152/ajpcell.00054.2011.Peer-Reviewed Original ResearchConceptsMM bathCation currentBath additionBath exposureOocyte studiesExpression increasesStrong hyperpolarizationFunction mutationsIntracellular pHElevated NaMembrane potentialOocytesDistinct cellular responsesFunction phenotypesInfluxPhenotypeCellular responsesAmine transportDistinct mechanismsElicit distinct cellular responsesPatients
2000
Gene transfer to ankyrin-deficient bone marrow corrects spherocytosis in vitro
Dooner G, Barker J, Gallagher P, Debatis M, Brown A, Forget B, Becker P. Gene transfer to ankyrin-deficient bone marrow corrects spherocytosis in vitro. Experimental Hematology 2000, 28: 765-774. PMID: 10907638, DOI: 10.1016/s0301-472x(00)00185-5.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAnkyrinsBlotting, WesternBone MarrowCell LineElectrophoresis, Polyacrylamide GelErythropoietinGene Transfer TechniquesGenetic TherapyHematopoietic Stem CellsHumansIn Vitro TechniquesMiceMice, Inbred BALB CRetroviridaeReverse Transcriptase Polymerase Chain ReactionSpherocytosis, HereditaryConceptsMEL cellsAnkyrin promoterGene transferDependence of expressionMurine bone marrow cellsMurine erythroleukemia cellsNormal murine bone marrow cellsRetroviral vectorsNbs mutantsMutant bone marrowMurine 3T3 fibroblastsNB cellsAnkyrin proteinsMutant cellsPolymerase chain reactionErythroid differentiation culturesHuman hemolytic anemiasColony polymerase chain reactionRT-PCRErythroid expressionBone marrow progenitorsErythroleukemia cellsDifferentiation culturesAnkyrinWestern blot analysis