2017
Sox17 drives functional engraftment of endothelium converted from non-vascular cells
Schachterle W, Badwe C, Palikuqi B, Kunar B, Ginsberg M, Lis R, Yokoyama M, Elemento O, Scandura J, Rafii S. Sox17 drives functional engraftment of endothelium converted from non-vascular cells. Nature Communications 2017, 8: 13963. PMID: 28091527, PMCID: PMC5260855, DOI: 10.1038/ncomms13963.Peer-Reviewed Original ResearchConceptsEndothelial cellsMorphogenesis genesETS transcription factorsVascular endothelial cellsTreat vasculopathyAmniotic cellsGenomic targetsConsensus sitesTransplantation strategiesInjured vesselsParacrine factorsTranscription factorsNon-vascular cellsSOX17 expressionVascular functionFunctional engraftmentTransplantation studiesGene expressionPromote tissue regenerationSOX17Support metabolismEnforced expressionEC-like cellsEC gene expressionTransplantation
2015
Sec63 and Xbp1 regulate IRE1α activity and polycystic disease severity
Fedeles SV, So JS, Shrikhande A, Lee SH, Gallagher AR, Barkauskas CE, Somlo S, Lee AH. Sec63 and Xbp1 regulate IRE1α activity and polycystic disease severity. Journal Of Clinical Investigation 2015, 125: 1955-1967. PMID: 25844898, PMCID: PMC4463201, DOI: 10.1172/jci78863.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCell LineDisease Models, AnimalDNA HelicasesDNA-Binding ProteinsEndoribonucleasesFemaleGlucosidasesIntracellular Signaling Peptides and ProteinsKidneyMaleMiceMice, Inbred C57BLMice, KnockoutMice, TransgenicMolecular ChaperonesPolycystic Kidney, Autosomal DominantPolycystic Kidney, Autosomal RecessiveProtein Serine-Threonine KinasesProtein Structure, TertiaryReceptors, G-Protein-CoupledRecombinant Fusion ProteinsRegulatory Factor X Transcription FactorsRNA SplicingRNA-Binding ProteinsRNA, Small InterferingTranscription FactorsTransfectionTRPP Cation ChannelsUnfolded Protein ResponseX-Box Binding Protein 1ConceptsG protein-coupled receptor proteolysis siteCyst formationPolycystic liver diseaseGPS cleavagePolycystin-1IRE1α-XBP1 branchMurine genetic modelsPolycystic kidney phenotypeLiver diseasePolycystic diseaseCystic diseaseDisease manifestationsMurine modelDisease severityKidney phenotypeXBP1 activationUnfolded protein response pathwayDiseaseXBP1 overexpressionPC1 functionsProtein response pathwayEnforced expressionMiceXBP1Activation of XBP1
1999
Recruitment of an alternatively spliced form of synaptojanin 2 to mitochondria by the interaction with the PDZ domain of a mitochondrial outer membrane protein
Nemoto Y, De Camilli P. Recruitment of an alternatively spliced form of synaptojanin 2 to mitochondria by the interaction with the PDZ domain of a mitochondrial outer membrane protein. The EMBO Journal 1999, 18: 2991-3006. PMID: 10357812, PMCID: PMC1171381, DOI: 10.1093/emboj/18.11.2991.Peer-Reviewed Original ResearchMeSH KeywordsAlternative SplicingAmino Acid SequenceAnimalsBase SequenceBinding SitesCarrier ProteinsCHO CellsCloning, MolecularCricetinaeCytoplasmExonsIntracellular MembranesIsoenzymesMembrane ProteinsMitochondriaMolecular Sequence DataMutationNerve Tissue ProteinsPhosphoric Monoester HydrolasesProtein BindingRatsRecombinant Fusion ProteinsRNA, MessengerYeastsConceptsMitochondrial outer membrane proteinMitochondrial outer membraneOuter membrane proteinsPDZ domainMembrane proteinsSynaptojanin 2Outer membraneNovel mitochondrial outer membrane proteinC-terminal transmembrane regionSingle PDZ domainPerinuclear clusteringTransmembrane regionSynaptojanin 1C-terminusExon sequencesSpliced formsEnforced expressionUnique motifModulation of inositolIntracellular distributionSynaptic vesiclesMitochondriaPutative roleOmp25Protein
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