grant
Control of allelic Gsα expression for regulating hormone signaling
Organization MASSACHUSETTS GENERAL HOSPITALLocation BOSTON, UNITED STATESPosted 2 Sept 2024Deadline 31 Jul 2028
NIHUS FederalResearch GrantFY2025AffectAlbright hereditary osteodystrophyAlbright syndrome 1AllelesAllelomorphsAutocrine SystemsBlood SerumBody TissuesBone DevelopmentCRISPRCRISPR/Cas systemCalciumCell BodyCell Communication and SignalingCell DifferentiationCell Differentiation processCell SignalingCell modelCellsCellular modelChondrocytesClinical ManagementClustered Regularly Interspaced Short Palindromic RepeatsCodeCoding SystemComplexDNA mutationDefectDiseaseDisorderEctopic OssificationEmbryoEmbryonicEndocrine Gland SecretionEnhancersEpiphyseal PlateEpiphysial cartilageExonsFuller Albright syndrome 1G(s), alpha SubunitG(s), α SubunitG(s)alphaG(s)αG-ProteinsGNAS geneGNAS1GNASXLGTP-Binding Protein alpha Subunits, GsGTP-Binding Protein α Subunits, GsGTP-Binding ProteinsGTP-Regulatory ProteinsGene AbnormalityGene DeletionGene TranscriptionGeneralized GrowthGenesGeneticGenetic ChangeGenetic TranscriptionGenetic defectGenetic mutationGrowthGrowth PlateGs alpha Family G-ProteinGsαGuanine Nucleotide Coupling ProteinGuanine Nucleotide Regulatory ProteinsGαsHeterotopic OssificationHormone ResponsiveHormonesHumanHypocalcemiaHypothyroidismImpairmentIntellectual disabilityIntellectual functioning disabilityIntellectual limitationIntermediary MetabolismIntracellular Communication and SignalingKnowledgeMediatingMetabolic ProcessesMetabolismMethylationModern ManMutationNESP55Nerve Transmitter SubstancesNeurotransmittersObesityOrganOsteoblastsPHP1APHP1BPTH geneParathyrinParathyroid HormonePathogenesisPathologic OssificationPathological OssificationPatientsPhenotypePhosphatesPlayProductionProximal Kidney TubulesPseudohypoparathyroidismPublishingRNA ExpressionRecombinant TSHRecombinant Thyroid-Stimulating HormoneRecurrenceRecurrentRegulationRegulatory Ns ProteinResistanceRoleSeabright Bantam syndromeSerumSignal TransductionSignal Transduction SystemsSignalingSignaling Factor Proto-OncogeneSignaling Pathway GeneSignaling ProteinSkeletal DevelopmentStimulatory Gs G-ProteinTestingTherapeuticTherapeutic HormoneThyreotropinThyroidThyroid GlandThyroid Head and NeckThyroid Stimulating HormoneThyroid-Stimulating HormoneThyrotropinTissue DifferentiationTissue GrowthTissuesTranscriptTranscriptionadiposityalpha Subunit Stimulatory GTP-Binding Proteinalpha-Gsautocrinebiological signal transductioncellular differentiationclinical significanceclinically significantcorpulencecurative interventioncurative therapeuticcurative therapycurative treatmentsderepressiongene deletion mutationgene functiongenome mutationhESChESC modelhormonal signalshormone resistancehormone signalshuman ES cellhuman ESChuman diseasehuman embryonic stem cellhuman embryonic stem cell based modelhuman embryonic stem cell derived modelhuman embryonic stem cell modeliPSiPSCiPSCsimprintimprovedinduced pluripotent cellinduced pluripotent stem cellinducible pluripotent cellinducible pluripotent stem cellinorganic phosphateintellectual and developmental disabilitylimited intellectual functioningloss of functionontogenyparacrineparathormonepreventpreventingpseudohypoparathyroidism syndromerenal proximal tubuleresistantsocial roletoolα-Gs
Description preview
Abstract
The α-subunit of the stimulatory G protein (Gsα) mediates the signaling of many hormones, autocrine/paracrine
factors, and neurotransmitters. Gsα and its gene, the GNAS complex locus, are central to many human disorders
with perturbed hormone actions and skeletal development. A distinctive way Gsα signaling is regulated involves
the…
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