grant
ENPP1 regulation of mammalian bone mass
NIHUS FederalResearch GrantFY202621+ years oldAdolescentAdolescent YouthAdultAdult HumanAgingAnimal ModelAnimal Models and Related StudiesAutomobile DrivingBioavailabilityBiochemicalBiologicalBiological AgentBiological AvailabilityBiological MarkersBiological ProductsBlood PlasmaBody TissuesBone DiseasesBone GrowthBone MatrixBone MineralizationCalcifiedCalcitriolCatalysisCell BodyCell Communication and SignalingCell SignalingCellsChronic Kidney FailureChronic Renal DiseaseChronic Renal FailureClinicCulturing, in vitro Vertebrate, PrimaryDNA mutationDataDevelopmentDietDiseaseDisorderENPP1 proteinEarly-onset osteoporosisEngineeringEnzyme GeneEnzymesExhibitsExperimental DesignsFamilial hypophosphatemic bone diseaseFractureGene TranscriptionGeneralized GrowthGeneticGenetic ChangeGenetic TranscriptionGenetic TransductionGenetic defectGenetic mutationGoalsGrowthHereditaryHistoryHumanHypophosphatemic RicketsInheritedIntracellular Communication and SignalingInvestigationKidneyKidney Urinary SystemLigamentsMammaliaMammalsMedicalMiceMice MammalsMineralsModern ManMolecularMorbidityMurineMusMutationNational Institutes of HealthOrganOsteoporosisPC-1 glycoproteinPathway interactionsPatient AgentsPatientsPhenotypePhosphatesPhysiologic AvailabilityPhysiologic OssificationPhysiologic calcificationPhysiological OssificationPlasmaPlasma SerumPopulationPrimary Cell CulturesProtein Replacement TherapyProteomicsPublic HealthPublicationsRNA ExpressionRecording of previous eventsRegulationRegulatory PathwayReportingResearchReticuloendothelial System, Serum, PlasmaRiskScientific PublicationSignal PathwaySignal TransductionSignal Transduction PathwaySignal Transduction SystemsSignalingSignaling Factor Proto-OncogeneSignaling Pathway GeneSignaling ProteinSkeletonSupplementationSurvival RateTendon structureTendonsTherapeuticTherapeutic AgentsTissue GrowthTissuesTranscriptionTransgenic MiceUnited States National Institutes of HealthVitamin D-Resistant RicketsX linked hypophosphatemia in ricketsX-Linked Hypophosphatemic RicketsX-linked hypophosphatemiaadulthoodarterial calcification of infancyautosomebench bed sidebench bedsidebench to bed sidebench to bedsidebench to clinicbench to clinical practicebio-markersbiologicbiologic markerbiological signal transductionbiologicsbiomarkerbiopharmaceuticalbiotherapeutic agentbonebone disorderbone fracturebone fragilitybone lossbone masscalcificationcandidate identificationchronic kidney diseaseconventional therapyconventional treatmentdesigndesigningdevelopmentaldietsdrivingearly onsetecto-nucleotide pyrophosphatase phosphodiesterase 1ectonucleotide pyrophosphatase phosphodiesterase 1enzyme replacement therapyenzyme replacement treatmentexperimentexperimental researchexperimental studyexperimentsfamilial hypophosphatemia in ricketsfracture riskgenome mutationhistorieshypophosphatemia in ricketsin vivoinhibitorinorganic phosphatejuvenilejuvenile humanmineralizationmodel of animalmortalitymouse modelmurine modelnormal ossificationnovelnucleotide pyrophosphatase-alkaline phosphodiesterase Iontogenyossificationpathwayplasma cell membrane glycoprotein PC-1posterior longitudinal ligament calcificationposterior longitudinal ligament ossificationrenalresponseskeletalskeletal diseaseskeletal disorderskeletonssoft tissuesuccesstranslational study
Description preview
Inactivating
including
Ligament
early-onset
mutations in human ENPP1 results in aberrant soft tissue and skeletal mineralization disorders,
Autosomal Recessive Hypophosphatemic Rickets (ARHR2) Ossification of the Posterior Longitudinal
(OPLL), and Generalized Arterial Calcification of Infancy (GACI) in homozygous deficiency, and
osteoporosis…
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