2013
Enhanced Fasting Glucose Turnover in Mice with Disrupted Action of TUG Protein in Skeletal Muscle*
Löffler MG, Birkenfeld AL, Philbrick KM, Belman JP, Habtemichael EN, Booth CJ, Castorena CM, Choi CS, Jornayvaz FR, Gassaway BM, Lee HY, Cartee GD, Philbrick W, Shulman GI, Samuel VT, Bogan JS. Enhanced Fasting Glucose Turnover in Mice with Disrupted Action of TUG Protein in Skeletal Muscle*. Journal Of Biological Chemistry 2013, 288: 20135-20150. PMID: 23744065, PMCID: PMC3711282, DOI: 10.1074/jbc.m113.458075.Peer-Reviewed Original ResearchMeSH Keywords3T3-L1 CellsAdaptor Proteins, Signal TransducingAnimalsBlood GlucoseCarbon DioxideCarrier ProteinsDeoxyglucoseFastingFemaleGlucoseGlucose Transporter Type 4GlycogenGolgi Matrix ProteinsHypoglycemic AgentsImmunoblottingInsulinIntracellular Signaling Peptides and ProteinsMaleMiceMice, Inbred C57BLMice, Inbred StrainsMice, TransgenicMuscle, SkeletalOxygen ConsumptionProtein TransportProteolysisConceptsGLUT4 translocationGLUT4 glucose transportersMuscle-specific transgenic expressionTransgenic miceT-tubule fractionTUG ProteinInsulin signalSystemic glucose homeostasisDiet-induced insulin resistanceHigh-fat diet-induced insulin resistanceEndoproteolytic cleavageTransgenic expressionTransgenic muscleGlucose transporterCell surfaceEnergy metabolismProteolysisTranslocationGLUT4Skeletal muscleGlucose uptakeHyperinsulinemic clamp studiesExpressionMetabolic rateTurnover
2001
Insulin secretion and IP levels in two distant lineages of the genus Mus: comparisons with rat islets
Zawalich W, Zawalich K, Tesz G, Sterpka J, Philbrick W. Insulin secretion and IP levels in two distant lineages of the genus Mus: comparisons with rat islets. AJP Endocrinology And Metabolism 2001, 280: e720-e728. PMID: 11287354, DOI: 10.1152/ajpendo.2001.280.5.e720.Peer-Reviewed Original Research
1996
Targeted overexpression of parathyroid hormone-related peptide in chondrocytes causes chondrodysplasia and delayed endochondral bone formation.
Weir E, Philbrick W, Amling M, Neff L, Baron R, Broadus A. Targeted overexpression of parathyroid hormone-related peptide in chondrocytes causes chondrodysplasia and delayed endochondral bone formation. Proceedings Of The National Academy Of Sciences Of The United States Of America 1996, 93: 10240-10245. PMID: 8816783, PMCID: PMC38368, DOI: 10.1073/pnas.93.19.10240.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBone DevelopmentDwarfismGene Expression Regulation, DevelopmentalGrowth PlateHumansMiceMice, Inbred C57BLMice, Inbred StrainsMice, TransgenicOsteochondrodysplasiasParathyroid HormoneParathyroid Hormone-Related ProteinPolymerase Chain ReactionProcollagenPromoter Regions, GeneticProtein BiosynthesisProteinsRegulatory Sequences, Nucleic AcidTranscription, GeneticConceptsPTH/PTHrP receptorHormone-related peptideParathyroid hormonePTHrP receptorParathyroid hormone-related peptideChondrocyte differentiationOverexpression of PTHrPType II collagen promoterEndochondral ossificationShort-limbed dwarfismParaneoplastic hypercalcemiaPTHrP functionsBone collar formationMalignant tumorsDevelopmental regulatory moleculeEndochondral bone formationTransgenic micePTHrPCommon receptorEndochondral bone developmentTargeted overexpressionFetal tissuesPTHrP geneFollicle formationNormal bone
1989
Functional and Molecular Changes in Colony Stimulating Factor Secretion by Osteoblasts
Horowitz M, Einhorn T, Philbrick W, Yale R. Functional and Molecular Changes in Colony Stimulating Factor Secretion by Osteoblasts. Connective Tissue Research 1989, 20: 159-168. PMID: 2558840, DOI: 10.3109/03008208909023884.Peer-Reviewed Original Research