2021
YAP1 nuclear efflux and transcriptional reprograming follow membrane diminution upon VSV-G-induced cell fusion
Feliciano D, Ott CM, Espinosa-Medina I, Weigel AV, Benedetti L, Milano KM, Tang Z, Lee T, Kliman HJ, Guller SM, Lippincott-Schwartz J. YAP1 nuclear efflux and transcriptional reprograming follow membrane diminution upon VSV-G-induced cell fusion. Nature Communications 2021, 12: 4502. PMID: 34301937, PMCID: PMC8302681, DOI: 10.1038/s41467-021-24708-2.Peer-Reviewed Original ResearchMeSH KeywordsAdaptor Proteins, Signal TransducingAMP-Activated Protein KinasesAnimalsBiological TransportCell FusionCell LineCell Line, TumorCell MembraneCell NucleusCells, CulturedGiant CellsHEK293 CellsHumansMembrane GlycoproteinsMiceRNA-SeqSignal TransductionTranscription FactorsTranscription, GeneticViral Envelope ProteinsYAP-Signaling ProteinsConceptsCell cycle arrestCell fusionNew cellular statesPlasma membrane surface areaRNA-seq analysisCell fusion systemTranscriptional programsNutrient stressCellular statesTranscriptional changesNuclear effluxCytoplasmic glucoseExtrinsic cuesUndifferentiated cellsGlucose transporterFused cellsMechanistic insightsMembrane surface areaNew functionsEndocytosisYAP1 inhibitionEnergetic stateSyncytiaCellsVSV
2018
hCALCRL mutation causes autosomal recessive nonimmune hydrops fetalis with lymphatic dysplasia
Mackie DI, Al Mutairi F, Davis RB, Kechele DO, Nielsen NR, Snyder JC, Caron MG, Kliman HJ, Berg JS, Simms J, Poyner DR, Caron KM. hCALCRL mutation causes autosomal recessive nonimmune hydrops fetalis with lymphatic dysplasia. Journal Of Experimental Medicine 2018, 215: 2339-2353. PMID: 30115739, PMCID: PMC6122977, DOI: 10.1084/jem.20180528.Peer-Reviewed Original ResearchConceptsStructure-function insightsG protein-coupled receptorsNovel candidate genesFirst extracellular loopProtein-coupled receptorsReceptor activity modifying proteinMutant resultsPlasma membraneCandidate genesGenetic mouse modelsExtracellular loopFrame deletionBiochemical assaysGenetic ablationReceptor chaperoneLymphatic endothelialModifying proteinsCalcitonin receptor-like receptorHuman physiologyEmbryonic demiseChaperonesMouse modelLymphatic dysplasiaReceptorsGenes