grant
Role of Protein Tyrosine Phosphatase 1B in Cardiac Hypertrophy
Organization STATE UNIVERSITY OF NEW YORK AT ALBANYLocation ALBANY, UNITED STATESPosted 15 Jun 2024Deadline 31 May 2028
NIHUS FederalResearch GrantFY20251-Phosphatidylinositol 3-KinaseAKTActive OxygenAdeno-Associated VirusesAffectAkt proteinBindingCardiac Muscle CellsCardiac MyocytesCardiocyteCell BodyCell Communication and SignalingCell SignalingCellsComplexDataDependoparvovirusDependovirusDephosphorylationDevelopmentDysfunctionEctopic ExpressionEventFunctional disorderGene Down-RegulationGene ExpressionGeneralized GrowthGrowthHeartHeart HypertrophyHeart Muscle CellsHeart failureHeart myocyteHormone ResponsiveHypertrophyIndividualIntracellular Communication and SignalingKO miceKnock-out MiceKnockout MiceKnowledgeL-TriiodothyronineLeft Ventricular FunctionLeft Ventricular HypertrophyLiothyronineMediatingMediatorMiceMice MammalsMolecularMolecular InteractionMurineMusMuscle CellsMyocardialMyocytesNatureNuclearNull MouseOxidantsOxidative StressOxidizing AgentsOxygen RadicalsPI-3 KinasePI3-KinasePI3CGPI3KGammaPI3kPIK3PIK3CGPIK3CG genePTP-1B proteinPTP1B enzymePathologicPathway interactionsPatientsPeptidesPhenotypePhosphatidylinositol 3-KinasePhosphatidylinositol-3-OH KinasePhosphoinositide 3-HydroxykinasePhosphorylationPhosphotyrosinePhysiopathologyPlayPost-Transcriptional ControlPost-Transcriptional RegulationPrevalencePro-OxidantsProtein DephosphorylationProtein Kinase BProtein PhosphorylationProteinsProto-Oncogene Proteins c-aktPtdIns 3-KinasePublic HealthPublishingRAC-PK proteinReactive Oxygen SpeciesRegulationRepressionResearchResponse ElementsRoleSeriesSeveritiesSignal TransductionSignal Transduction SystemsSignalingSourceSyndromeT-3T3 Thyroid HormoneTestingTherapeuticTherapeutic InterventionTherapeutic T3Therapeutic TriiodothyronineThyroid Gland HormoneThyroid Hormone ReceptorThyroid HormonesTissue GrowthTranscription RepressionTranscriptional ControlTranscriptional RegulationTranslatingTriiodothyronineType I Phosphatidylinositol KinaseType III Phosphoinositide 3-KinaseTyrosineTyrosine-O-phosphateUnited StatesWorkadeno associated virus groupbiological signal transductionc-akt proteincardiac failurecardiac hypertrophycardiomyocytecardioprotectantcardioprotectioncardioprotectivedevelopmentalelectron acceptorexperimentexperimental researchexperimental studyexperimentsfunctional restorationgene repressionhormonal signalshormone signalsimprovedin vivoinsightintervention therapyknock-downknockdownnew therapeutic approachnew therapeutic interventionnew therapeutic strategiesnew therapy approachesnew treatment approachnew treatment strategynon-genomicnongenomicnovelnovel therapeutic approachnovel therapeutic interventionnovel therapeutic strategiesnovel therapy approachontogenyoxidationpathophysiologypathwaypharmacologicpost-transcriptional gene regulationposttranscriptionalpressurepreventpreventingprotein tyrosine phosphatase 1Bproto-oncogene protein RACproto-oncogene protein aktrac protein kinaserelated to A and C-proteinrestore functionrestore functionalityrestore lost functionsocial roletooltranslation factortreatment guidelines
Description preview
Project Summary
Oxidative stress is associated with reduced left ventricular (LV) function and correlates with the severity of heart
failure in patients. We have recently demonstrated that Protein Tyrosine Phosphatase 1B (PTP1B) becomes
reversibly oxidized and inactivated in pressure overload-induced cardiac hypertrophy and that PTP1B
inactivation…
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