2015
Expression of the CTCFL Gene during Mouse Embryogenesis Causes Growth Retardation, Postnatal Lethality, and Dysregulation of the Transforming Growth Factor β Pathway
Sati L, Zeiss C, Yekkala K, Demir R, McGrath J. Expression of the CTCFL Gene during Mouse Embryogenesis Causes Growth Retardation, Postnatal Lethality, and Dysregulation of the Transforming Growth Factor β Pathway. Molecular And Cellular Biology 2015, 35: 3436-3445. PMID: 26169830, PMCID: PMC4561735, DOI: 10.1128/mcb.00381-15.Peer-Reviewed Original ResearchConceptsGrowth factor β pathwayHuman vascular malformationsTestis-expressed genesΒ pathwayParalog of CTCFEmbryonic stem cellsTransforming Growth Factor-β PathwayPrior mouse modelsMouse embryogenesisBioinformatics analysisCancer-testis antigensDownstream targetsES cellsPostnatal lethalityCTCFLEmbryogenesis resultsTGFB pathwayGenesStem cellsVascular defectsPathwayExpressionTransgenic miceEye malformationsPhenotype
2014
Hypothalamic prolyl endopeptidase (PREP) regulates pancreatic insulin and glucagon secretion in mice
Kim JD, Toda C, D’Agostino G, Zeiss CJ, DiLeone RJ, Elsworth JD, Kibbey RG, Chan O, Harvey BK, Richie CT, Savolainen M, Myöhänen T, Jeong JK, Diano S. Hypothalamic prolyl endopeptidase (PREP) regulates pancreatic insulin and glucagon secretion in mice. Proceedings Of The National Academy Of Sciences Of The United States Of America 2014, 111: 11876-11881. PMID: 25071172, PMCID: PMC4136568, DOI: 10.1073/pnas.1406000111.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBlood GlucoseGene ExpressionGene Knockdown TechniquesGlucagonGlucose Clamp TechniqueGlucose IntoleranceHypothalamusIndolesInsulinInsulin SecretionIon ChannelsMaleMiceMice, TransgenicMitochondrial ProteinsPancreasPhosphorylationProlyl OligopeptidasesReceptor, InsulinRecombinant ProteinsSerine EndopeptidasesSerine Proteinase InhibitorsThiazolidinesUncoupling Protein 1Ventromedial Hypothalamic NucleusConceptsWild-type miceGlucose intoleranceGlucagon secretionProlyl endopeptidaseHyperinsulinemic-euglycemic clamp studiesWild-type control miceGlucose-induced insulin releaseGlucose-induced insulin secretionEuglycemic clamp studiesAutonomic nervous systemVMH injectionsSympathetic outflowWild-type controlsNorepinephrine levelsGlucagon levelsGlucose toleranceControl miceInsulin levelsCentral infusionPancreatic functionVentromedial nucleusInsulin secretionNeuronal activationGlucose-intolerant phenotypeCentral regulation
2005
Correlation of tumor phenotype with c-fms proto-oncogene expression in an in vivo intraperitoneal model for experimental human breast cancer metastasis
Toy EP, Bonafé N, Savlu A, Zeiss C, Zheng W, Flick M, Chambers SK. Correlation of tumor phenotype with c-fms proto-oncogene expression in an in vivo intraperitoneal model for experimental human breast cancer metastasis. Clinical & Experimental Metastasis 2005, 22: 1-9. PMID: 16132573, DOI: 10.1007/s10585-005-0718-4.Peer-Reviewed Original ResearchConceptsBALB/cProto-oncogene expressionC-fms proto-oncogene expressionExpression groupAthymic BALB/cHuman breast cancer metastasisIntraperitoneal modelBreast cancer metastasisHuman breast carcinoma cellsBreast carcinoma cellsClinical outcomesClinical evidenceTumor sizeC-fmsIntrasplenic injectionPrimary tumorMetastatic spreadOral administrationRU 486SCID miceBreast carcinomaSCID animalsImmunodeficient miceIHC stainingNovel treatments