William Philbrick, PhD
Senior Research ScientistDownloadHi-Res Photo
Cards
Appointments
Endocrinology
Primary
Additional Titles
Director, Diabetes Endocrinology Research Center Molecular Core
Contact Info
Appointments
Endocrinology
Primary
Additional Titles
Director, Diabetes Endocrinology Research Center Molecular Core
Contact Info
Appointments
Endocrinology
Primary
Additional Titles
Director, Diabetes Endocrinology Research Center Molecular Core
Contact Info
About
Titles
Senior Research Scientist
Director, Diabetes Endocrinology Research Center Molecular Core
Appointments
Endocrinology
Senior Research ScientistPrimary
Other Departments & Organizations
- Diabetes Research Center
- Endocrinology
- Internal Medicine
- Yale Genome Editing Center (YGEC)
Education & Training
- PhD
- SUNY at Buffalo (1985)
- Postdoctoral Fellow
- Yale University School of Medicine
Research
Overview
Medical Research Interests
Diabetes Mellitus; Endocrinology; Parathyroid Hormone-Related Protein
Research at a Glance
Yale Co-Authors
Frequent collaborators of William Philbrick's published research.
Publications Timeline
A big-picture view of William Philbrick's research output by year.
Research Interests
Research topics William Philbrick is interested in exploring.
John Wysolmerski, MD
Paula Preston-Hurlburt
Smita Krishnaswamy, PhD
Akiko Iwasaki, PhD
Huiping Dong
Karl Insogna, MD, FACP
24Publications
2,637Citations
Parathyroid Hormone-Related Protein
Publications
2023
HSV-2 triggers upregulation of MALAT1 in CD4+ T cells and promotes HIV latency reversal
Pierce C, Loh L, Steach H, Cheshenko N, Preston-Hurlburt P, Zhang F, Stransky S, Kravets L, Sidoli S, Philbrick W, Nassar M, Krishnaswamy S, Herold K, Herold B. HSV-2 triggers upregulation of MALAT1 in CD4+ T cells and promotes HIV latency reversal. Journal Of Clinical Investigation 2023, 133: e164317. PMID: 37079384, PMCID: PMC10232005, DOI: 10.1172/jci164317.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsHIV-1 reactivationHIV latency reversalT cellsLatency reversalHuman CD4HIV-1 viral loadHIV-1 restriction factorsHSV-2 recurrencesHSV-2 infectionHIV-1 latencyUpregulation of MALAT1Primary human CD4HSV-2 proteinsViral loadHIV replicationPeripheral bloodMALAT1 expressionHSV-2Tissue reservoirsCD4Viral replicationExpression of transcriptsBystander cellsRestriction factorsMALAT1
2022
HSV-2 increases replication of HIV in human T cells
Pierce C, Preston-Hurlburt P, Loh L, Steach H, Sidoli S, Zhang F, Philbrick W, Nassar M, Krishnaswamy S, Herold K, Herold B. HSV-2 increases replication of HIV in human T cells. The Journal Of Immunology 2022, 208: 182.40-182.40. DOI: 10.4049/jimmunol.208.supp.182.40.Peer-Reviewed Original ResearchConceptsCD4 cellsHSV-2HIV reactivationHIV PVLT cellsHerpes simplex virus 2 infectionLncRNA MALAT1Simplex virus 2 infectionHIV-LTR expressionHSV-2 lesionsMALAT1 gene expressionUninfected CD4 cellsFollicular helper cellsHSV-2 infectionCD4 T cellsHIV restriction factorsVirus 2 infectionGlobal HIV epidemicHSV-2 glycoprotein BHIV latent reservoirHuman T cellsInterferon response genesMucosal responsesHSV infectionLatent reservoir
2021
Endogenous retroviruses mediate IFN-independent protection against vaginal HSV-2 infection
Tokuyama M, Jayewickreme R, Mao T, Philbrick W, Kong Y, Dong H, Treger R, Rakib T, Iwasaki A. Endogenous retroviruses mediate IFN-independent protection against vaginal HSV-2 infection. The Journal Of Immunology 2021, 206: 20.39-20.39. DOI: 10.4049/jimmunol.206.supp.20.39.Peer-Reviewed Original ResearchConceptsHSV-2 infectionVaginal HSV-2 infectionTight junction proteinsB6 miceVaginal epitheliumHerpes simplex virus type 2 infectionSimplex virus type 2 infectionEnhanced type I interferonIntravaginal HSV-2 infectionVirus type 2 infectionToll-like receptor 7Epithelial tight junction proteinsEndogenous retrovirusesReceptor-deficient miceJunction proteinsType 2 infectionHigh systemic levelsWildtype C57BL/6 miceType I interferonDisease courseC57BL/6 miceInfectious endogenous retrovirusReceptor 7Disease burdenHSV-2
2014
NLRP6 Inflammasome Orchestrates the Colonic Host-Microbial Interface by Regulating Goblet Cell Mucus Secretion
Wlodarska M, Thaiss CA, Nowarski R, Henao-Mejia J, Zhang JP, Brown EM, Frankel G, Levy M, Katz MN, Philbrick WM, Elinav E, Finlay BB, Flavell RA. NLRP6 Inflammasome Orchestrates the Colonic Host-Microbial Interface by Regulating Goblet Cell Mucus Secretion. Cell 2014, 156: 1045-1059. PMID: 24581500, PMCID: PMC4017640, DOI: 10.1016/j.cell.2014.01.026.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsRegulatory pathwaysGoblet cell mucus secretionHost-microbial mutualismHost-microbial interfaceNLRP6 inflammasomeMucus secretionGoblet cellsBiogeographical distributionProkaryotic cellsInnate immune playersNLRP6 deficiencyGranule exocytosisImmune regulatory pathwaysInflammasome-deficient miceColonic microbiota compositionLarge intestinal lumenCritical orchestratorsImmune playersPersistent infectionMucus productionCellsIntestinal lumenPathwayMucosal surfacesMicrobiota composition
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 ResearchCitationsAltmetricMeSH Keywords and ConceptsMeSH 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 ResearchCitationsMeSH Keywords and ConceptsAbsence of Functional Type 1 Parathyroid Hormone (PTH)/PTH-Related Protein Receptors in Humans Is Associated with Abnormal Breast Development and Tooth Impaction1
Wysolmerski J, Cormier S, Philbrick W, Dann P, Zhang J, Roume J, Delezoide A, Silve C. Absence of Functional Type 1 Parathyroid Hormone (PTH)/PTH-Related Protein Receptors in Humans Is Associated with Abnormal Breast Development and Tooth Impaction1. The Journal Of Clinical Endocrinology & Metabolism 2001, 86: 1788-1794. PMID: 11297619, DOI: 10.1210/jcem.86.4.7404.Peer-Reviewed Original ResearchCitationsMeSH Keywords and ConceptsConceptsParathyroid hormoneHuman breastBreast developmentType 1 PTH/PTHrP receptorBlomstrand chondrodysplasiaPTH/PTHrP receptorAbnormal breast developmentBone formationTooth developmentNormal human fetusesTooth impactionPTHrP receptorEndochondral bone formationTransgenic miceAlveolar boneHuman fetusesEndochondral bone developmentBreastSevere abnormalitiesEpithelial-mesenchymal interactionsLethal formMammary glandFetusesBone developmentTeethChapter 3 Parathyroid Hormone-Related Protein Gene Structure, Biosynthesis, Metabolism, and Regulation
Philbrick W. Chapter 3 Parathyroid Hormone-Related Protein Gene Structure, Biosynthesis, Metabolism, and Regulation. 2001, 31-51. DOI: 10.1016/b978-012098651-4/50005-5.Peer-Reviewed Original ResearchCitations
2000
βiv Spectrin, a New Spectrin Localized at Axon Initial Segments and Nodes of Ranvier in the Central and Peripheral Nervous System
Berghs S, Aggujaro D, Dirkx R, Maksimova E, Stabach P, Hermel J, Zhang J, Philbrick W, Slepnev V, Ort T, Solimena M. βiv Spectrin, a New Spectrin Localized at Axon Initial Segments and Nodes of Ranvier in the Central and Peripheral Nervous System. Journal Of Cell Biology 2000, 151: 985-1002. PMID: 11086001, PMCID: PMC2174349, DOI: 10.1083/jcb.151.5.985.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsMeSH KeywordsAmino Acid SequenceAnimalsAnkyrinsAutoantigensAxonsBlood ProteinsBrain ChemistryChromosomesCloning, MolecularCOS CellsCytoplasmCytoskeletonDiabetic NeuropathiesGene ExpressionHippocampusHumansIslets of LangerhansMaleMembrane ProteinsMiceMolecular Sequence DataNerve Tissue ProteinsPhosphoproteinsProtein Structure, TertiaryProtein Tyrosine PhosphatasesRanvier's NodesRatsRats, Sprague-DawleyReceptor-Like Protein Tyrosine Phosphatases, Class 8RNA, MessengerSciatic NerveSignal TransductionSodium ChannelsSpectrinConceptsPleckstrin homology domainHomology domainBetaIV spectrinActin-binding domainAxon initial segmentPutative SH3Alternative splicingSpectrin geneSpectrin repeatsDetergent extractabilityCell adhesion moleculeNodes of RanvierSubcellular fractionationTerminal halfAdditional isoformsDistinct isoformsLong isoformNorthern blotSpectrinAbundant expressionΒIV-spectrinIsoformsSpectrin antibodiesEmbryonic day 19Initial segmentParathyroid hormone-related protein induces spontaneous osteoclast formation via a paracrine cascade
Nakchbandi I, Weir E, Insogna K, Philbrick W, Broadus A. Parathyroid hormone-related protein induces spontaneous osteoclast formation via a paracrine cascade. Proceedings Of The National Academy Of Sciences Of The United States Of America 2000, 97: 7296-7300. PMID: 10829073, PMCID: PMC16539, DOI: 10.1073/pnas.110553397.Peer-Reviewed Original ResearchCitationsMeSH Keywords and ConceptsConceptsNumber of osteoclastsEffects of PTHrPOsteoclast formationDF cellsBone resorptionFactor expressionOsteoclastic bone resorptionDental follicle cellsHormone-related proteinOsteoclast differentiation factorStellate reticulum cellsOsteoclastogenesis inhibitory factorCoronal tooth surfacesSpontaneous osteoclast formationParacrine cascadeParathyroid hormoneEruption pathwayReticulum cellsPeripheral skeletonTooth eruptionOsteoclast precursorsPTH/PTHrP.Inhibitory factorFunctional osteoclastsCrypt cells
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