2024
Corrigendum to “PTH-dependent stabilization of RANKL mRNA is associated with increased phosphorylation of the KH-type splicing regulatory protein” [Molecul. Cellul. Endocrinol. 595 (2025) 112412]
Yao G, Zhu M, Insogna K. Corrigendum to “PTH-dependent stabilization of RANKL mRNA is associated with increased phosphorylation of the KH-type splicing regulatory protein” [Molecul. Cellul. Endocrinol. 595 (2025) 112412]. Molecular And Cellular Endocrinology 2024, 112429. PMID: 39616004, DOI: 10.1016/j.mce.2024.112429.Peer-Reviewed Original ResearchPTH-dependent stabilization of RANKL mRNA is associated with increased phosphorylation of the KH-type splicing regulatory protein
Yao G, Zhu M, Insogna K. PTH-dependent stabilization of RANKL mRNA is associated with increased phosphorylation of the KH-type splicing regulatory protein. Molecular And Cellular Endocrinology 2024, 595: 112412. PMID: 39536935, DOI: 10.1016/j.mce.2024.112412.Peer-Reviewed Original ResearchReceptor activator of nuclear factor kappa-B ligandReceptor activator of nuclear factor kappa-B ligand mRNAAU-rich elementsParathyroid hormone treatmentParathyroid hormoneMRNA stabilityRegulation of mRNA stabilityAU-rich element-binding proteinBinding to AU-rich elementsActivation of transcriptionInhibition of cellular transcriptionRegulate mRNA stabilityCells treated with vehicleSplicing regulatory proteinKH-type splicing regulatory proteinNuclear factor kappa-B ligandAu-richElement-binding proteinTNF family membersCellular transcriptionAssociated with increased phosphorylationPTH exposureRegulatory proteinsBinding proteinCells pre-treated
2023
Altered Expression of Several Molecular Mediators of Cerebrospinal Fluid Production in Hyp Mice
Kaplan J, Tommasini S, Yao G, Zhu M, Nishimura S, Ghazarian S, Louvi A, Insogna K. Altered Expression of Several Molecular Mediators of Cerebrospinal Fluid Production in Hyp Mice. Journal Of The Endocrine Society 2023, 7: bvad022. PMID: 36819458, PMCID: PMC9936957, DOI: 10.1210/jendso/bvad022.Peer-Reviewed Original Research
2021
An Unanticipated Role for Sphingosine Kinase-2 in Bone and in the Anabolic Effect of Parathyroid Hormone
Walker JM, Yao GQ, Siu E, Zhu M, Sun BH, Simpson C, Insogna KL. An Unanticipated Role for Sphingosine Kinase-2 in Bone and in the Anabolic Effect of Parathyroid Hormone. Endocrinology 2021, 162: bqab042. PMID: 33640975, PMCID: PMC8095390, DOI: 10.1210/endocr/bqab042.Peer-Reviewed Original ResearchConceptsSphk2-/- miceParathyroid hormoneAnabolic responseFemoral trabecular BV/TVLower spinal bone mineral densityTrabecular BV/TVSpinal bone mineral densityDaily parathyroid hormoneFemoral bone volumeSuppression of sclerostinEnd of treatmentNormal bone massBone mineral densityNormal bone remodelingRole of SphK1BV/TVFemale control animalsSphingosine kinase 2Sphingosine kinaseControl miceLow BMDAnabolic effectsBone massMineral densityControl animals
2020
Identification of a 22 bp DNA cis Element that Plays a Critical Role in Colony Stimulating Factor 1-Dependent Transcriptional Activation of the SPHK1 Gene
Yao GQ, Zhu M, Walker J, Insogna K. Identification of a 22 bp DNA cis Element that Plays a Critical Role in Colony Stimulating Factor 1-Dependent Transcriptional Activation of the SPHK1 Gene. Calcified Tissue International 2020, 107: 52-59. PMID: 32246175, PMCID: PMC7274855, DOI: 10.1007/s00223-020-00685-4.Peer-Reviewed Original ResearchConceptsColony stimulating factor 1Sphingosine kinase 1Bp fragmentSPHK1 promoterBp sequenceSphK1 geneDNA cis elementsProtein binding regionsSPHK1 gene expressionBp DNA fragmentStimulating factor 1Dual-luciferase reporterPutative DNATranscriptional activationTranscription factorsNuclear proteinsDNA sequencesCis elementsDNA bindingGene expressionPromoter activityDNA fragmentsKinase 1EMSAsProtein binding
2017
Selective deletion of the soluble Colony-Stimulating Factor 1 isoform in vivo prevents estrogen-deficiency bone loss in mice
Yao GQ, Troiano N, Simpson CA, Insogna KL. Selective deletion of the soluble Colony-Stimulating Factor 1 isoform in vivo prevents estrogen-deficiency bone loss in mice. Bone Research 2017, 5: 17022. PMID: 29152381, PMCID: PMC5684603, DOI: 10.1038/boneres.2017.22.Peer-Reviewed Original ResearchBone mineral densityEstrogen-deficiency bone lossBone lossO miceTotal bone mineral densityWild-type female miceDual-energy X-ray absorptiometryX-ray absorptiometrySham-OVXReverse transcription-PCRFemale miceMineral densityWT controlsOVXSelective deletionMiceTranscription-PCRSignificant differencesCSF1Bone tissueMicro-CTSkeletal tissuesTissueNon-redundant functionsAnimals
2016
An Unusual Case of Rickets and How Whole Exome Sequencing Helped to Correct a Diagnosis
Peter P, Brownstein C, Yao G, Olear E, Simpson C, Agrawal P, Carpenter T, Insogna K. An Unusual Case of Rickets and How Whole Exome Sequencing Helped to Correct a Diagnosis. AACE Clinical Case Reports 2016, 2: ee278-ee283. DOI: 10.4158/ep15944.cr.Peer-Reviewed Original ResearchWhole-exome sequencingForms of ricketsExome sequencingGrowth factor 23Classic clinical featuresClinical suspicionClinical featuresClinical presentationFactor 23Parathyroid hormoneDihydroxyvitamin D3Correct diagnosisMistaken diagnosisUnusual caseNutritional deficienciesRicketsPatientsDiagnosisDiseaseHypophosphatemiaGenetic defectsCompound heterozygotesCYP27B1Gene sequencing technologyXLH
2015
AgRP Neurons Regulate Bone Mass
Kim JG, Sun BH, Dietrich MO, Koch M, Yao GQ, Diano S, Insogna K, Horvath TL. AgRP Neurons Regulate Bone Mass. Cell Reports 2015, 13: 8-14. PMID: 26411686, PMCID: PMC5868421, DOI: 10.1016/j.celrep.2015.08.070.Peer-Reviewed Original ResearchMeSH KeywordsAgouti-Related ProteinAnimalsArcuate Nucleus of HypothalamusBone DensityBone Diseases, MetabolicFemurGene Expression RegulationHomeostasisHypothalamusIon ChannelsLeptinMaleMiceMice, KnockoutMitochondrial ProteinsNeuronsNorepinephrinePhenotypePropranololReceptors, Adrenergic, betaReceptors, LeptinSignal TransductionSirtuin 1TibiaUncoupling Protein 2ConceptsAgRP neuronsCell-autonomous deletionSignificant regulatory roleAgRP neuronal functionBone massLeptin receptor deletionSkeletal bone metabolismTransgenic animalsRegulatory roleGene deletionBone homeostasisDeletionNeuronal functionPostnatal deletionSympathetic toneReceptor deletionArcuate nucleusLeptin actionBone metabolismSkeletal metabolismMultiple linesNeuronsMiceMetabolismCircuit integrity
2014
The Transcription Factor T-box 3 Regulates Colony-stimulating Factor 1-dependent Jun Dimerization Protein 2 Expression and Plays an Important Role in Osteoclastogenesis*
Yao C, Yao GQ, Sun BH, Zhang C, Tommasini SM, Insogna K. The Transcription Factor T-box 3 Regulates Colony-stimulating Factor 1-dependent Jun Dimerization Protein 2 Expression and Plays an Important Role in Osteoclastogenesis*. Journal Of Biological Chemistry 2014, 289: 6775-6790. PMID: 24394418, PMCID: PMC3945339, DOI: 10.1074/jbc.m113.499210.Peer-Reviewed Original Research
2013
Increasing dietary protein selectively upregulates the DMT1 isoform that contains an iron responsive element
Thomas C, Yao G, O'Brien K, Kerstetter J, Insogna K. Increasing dietary protein selectively upregulates the DMT1 isoform that contains an iron responsive element. The FASEB Journal 2013, 27: lb284-lb284. DOI: 10.1096/fasebj.27.1_supplement.lb284.Peer-Reviewed Original ResearchIntestinal iron absorptionIron absorptionDietary proteinProtein dietMRNA expressionWhole-body iron homeostasisDuodenum of ratsDMT1 mRNA expressionBody iron homeostasisGenetic absenceExperimental animalsLevel of expressionResponsive elementBrush border membraneRatsIron-responsive elementRecent dataDietCritical regulatorIron homeostasisBorder membraneSignificant changesExpressionIron importerAnimals
2011
Selective deletion of the membrane-bound colony stimulating factor 1 isoform leads to high bone mass but does not protect against estrogen-deficiency bone loss
Yao GQ, Wu JJ, Troiano N, Zhu ML, Xiao XY, Insogna K. Selective deletion of the membrane-bound colony stimulating factor 1 isoform leads to high bone mass but does not protect against estrogen-deficiency bone loss. Journal Of Bone And Mineral Metabolism 2011, 30: 408-418. PMID: 22105655, PMCID: PMC4378684, DOI: 10.1007/s00774-011-0336-y.Peer-Reviewed Original ResearchAnimalsBone and BonesBone DensityCell DifferentiationCells, CulturedCoculture TechniquesColony-Stimulating FactorsFemaleHumansHypertriglyceridemiaMaleMiceMice, KnockoutOsteoblastsOsteoclastsOsteoporosisOsteoporosis, PostmenopausalProtein IsoformsRNA, MessengerSex CharacteristicsSolubilityUp-Regulation
2010
Targeted overexpression of Dkk1 in osteoblasts reduces bone mass but does not impair the anabolic response to intermittent PTH treatment in mice
Yao GQ, Wu JJ, Troiano N, Insogna K. Targeted overexpression of Dkk1 in osteoblasts reduces bone mass but does not impair the anabolic response to intermittent PTH treatment in mice. Journal Of Bone And Mineral Metabolism 2010, 29: 141-148. PMID: 20602130, PMCID: PMC3457021, DOI: 10.1007/s00774-010-0202-3.Peer-Reviewed Original ResearchConceptsParathyroid hormonePTH treatmentBone massTg miceAnabolic responseDKK1 expressionSingle daily subcutaneous doseDaily subcutaneous doseBone formationIntermittent PTH treatmentPotent anabolic agentOverexpression of DKK1Number of osteoblastsSubcutaneous doseWT miceReal-time PCRSkeletal sitesDickkopf-1Anabolic agentsBody weightTransgenic miceHistomorphometric parametersHistomorphometric analysisTargeted overexpressionPrimary murine osteoblasts
2009
Targeted overexpression of the two colony-stimulating factor-1 isoforms in osteoblasts differentially affects bone loss in ovariectomized mice
Yao GQ, Wu JJ, Ovadia S, Troiano N, Sun BH, Insogna K. Targeted overexpression of the two colony-stimulating factor-1 isoforms in osteoblasts differentially affects bone loss in ovariectomized mice. AJP Endocrinology And Metabolism 2009, 296: e714-e720. PMID: 19141689, PMCID: PMC2670621, DOI: 10.1152/ajpendo.90631.2008.Peer-Reviewed Original ResearchConceptsColony-stimulating factor-1Nonredundant functionsWild-type animalsTransgenic miceMembrane-bound isoformMCSF1Normal osteoclastogenesisCollagen promoterTransgenic expressionMajor isoformsIsoformsFactor 1Same genotypeOp phenotypeTargeted overexpressionOverexpressionOp miceOsteoblastsAnimalsPromoterMicePhenotypeFemale animalsAlphaIMale littermates
2005
The Cell-Surface Isoform of Colony Stimulating Factor 1 (CSF1) Restores but Does Not Completely Normalize Fecundity in CSF1-Deficient Mice1
Ovadia S, Insogna K, Yao GQ. The Cell-Surface Isoform of Colony Stimulating Factor 1 (CSF1) Restores but Does Not Completely Normalize Fecundity in CSF1-Deficient Mice1. Biology Of Reproduction 2005, 74: 331-336. PMID: 16237150, DOI: 10.1095/biolreprod.105.045047.Peer-Reviewed Original ResearchConceptsColony stimulating factor 1Viability of offspringReproductive defectsCell surfaceMembrane-bound isoformStimulating factor 1Cell surface isoformAlpha promoterMCSF1Transgenic animalsProteolytic sheddingCSF1 proteinMouse reproductionFactor 1ReproductionTransgenic male miceIsoformsTransgenic miceSperm numberOffspringTissue levelsMurine uterusGenetic absenceControl littermatesPromoterCSF-1 Induces fos Gene Transcription and Activates the Transcription Factor Elk-1 in Mature Osteoclasts
Yao G, Itokawa T, Paliwal I, Insogna K. CSF-1 Induces fos Gene Transcription and Activates the Transcription Factor Elk-1 in Mature Osteoclasts. Calcified Tissue International 2005, 76: 371-378. PMID: 15812575, DOI: 10.1007/s00223-004-0099-8.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAnimals, NewbornCell NucleusCells, CulturedDNA-Binding ProteinsEts-Domain Protein Elk-1Genes, fosMacrophage Colony-Stimulating FactorMiceMice, TransgenicOsteoclastsProto-Oncogene ProteinsProto-Oncogene Proteins c-fosRNA, MessengerTranscription FactorsTranscription, GeneticTranscriptional ActivationConceptsTranscription factor Elk-1Serum response elementTranscriptional activationElk-1CSF-1Response elementMature osteoclastsNuclear c-Fos proteinRegulation of FosBacterial lac Z geneC-fosSap-1aFos serum response elementFos promoterNuclear proteinsGene transcriptionFos geneMolecular mechanismsLac Z geneVehicle-treated cellsTargeted deletionFactor 1Absolute requirementC-Fos proteinLike cells
2003
The Cell Surface Form of Colony-Stimulating Factor-1 Is Biologically Active in Bone in Vivo
Yao GQ, Wu JJ, Sun BH, Troiano N, Mitnick MA, Insogna K. The Cell Surface Form of Colony-Stimulating Factor-1 Is Biologically Active in Bone in Vivo. Endocrinology 2003, 144: 3677-3682. PMID: 12865350, DOI: 10.1210/en.2002-221071.Peer-Reviewed Original ResearchConceptsOp/op miceWild-type miceOp miceBone densityTooth eruptionTransgenic micePeripheral quantitative computed tomographyMCSF-1Factor 1Number of osteoclastsQuantitative computed tomographyOp/op animalsMolar tooth eruptionWild-type animalsOP animalsComputed tomographyColony-stimulating factor-1Colony stimulating factor 1Normal incisorsHistomorphometric analysis
2002
A Role for Cell-Surface CSF-1 in Osteoblast-mediated Osteoclastogenesis
Yao G, Sun BH, Weir EC, Insogna KL. A Role for Cell-Surface CSF-1 in Osteoblast-mediated Osteoclastogenesis. Calcified Tissue International 2002, 70: 339-346. PMID: 12004339, DOI: 10.1007/s00223-001-1079-x.Peer-Reviewed Original Research
2000
Nuclear Factor-κB p50 Is Required for Tumor Necrosis Factor-α-Induced Colony-Stimulating Factor-1 Gene Expression in Osteoblasts*
Yao G, Sun B, Insogna K, Weir E. Nuclear Factor-κB p50 Is Required for Tumor Necrosis Factor-α-Induced Colony-Stimulating Factor-1 Gene Expression in Osteoblasts*. Endocrinology 2000, 141: 2914-2922. PMID: 10919279, DOI: 10.1210/endo.141.8.7592.Peer-Reviewed Original ResearchConceptsCSF-1 expressionGene expressionElectrophoretic mobility shift assaysCSF-1 promoterCSF-1 gene expressionMobility shift assaysInducible complexTranscriptional mechanismsShift assaysNuclear factor-κB p50Northern analysisNF-kappaB p50NF-kappaB siteCSF-1Messenger RNAC-RelBcl-3Rel BRNA expressionTNF treatmentHematopoietic growth factorsMessenger RNA expressionIkappaB-alphaOsteoblastsNF-kappaBNuclear Factor-κB p50 Is Required for Tumor Necrosis Factor-α-Induced Colony-Stimulating Factor-1 Gene Expression in Osteoblasts*
Yao G, Sun B, Insogna K, Weir E. Nuclear Factor-κB p50 Is Required for Tumor Necrosis Factor-α-Induced Colony-Stimulating Factor-1 Gene Expression in Osteoblasts*. Endocrinology 2000, 141: 2914-2922. DOI: 10.1210/en.141.8.2914.Peer-Reviewed Original ResearchCSF-1 expressionKnock-out miceCSF-1NF-kBColony-stimulating factor (CSF)-1Gene expressionColony-stimulating factor-1 gene expressionCSF-1 gene expressionElectrophoretic mobility shift assayTumor necrosis factor (TNF)-aBone-resorbing agentsHematopoietic growth factorsWild-type miceMobility shift assayCSF-1 promoterBone remodeling in vivoNF-kB bindingNF-kB sitesMessenger RNA expressionShift assaysRemodeling in vivoTranscriptional mechanismsNorthern analysisBcl-3C-RelColony Stimulating Factors and Bone. In: Skeletal Growth Factors
1. Weir EC, Yao GQ, Chen Y, Insogna K: Colony Stimulating Factors and Bone. In: Skeletal Growth Factors. Canalis, E. (ed.), Lippincott Williams& Wilkins, Media, PA 2000, p385-409Chapters