grant
The roles of p53 and MYC dynamics in regulating heterogeneous cell fate responses to genotoxic stress
Organization UNIVERSITY OF MINNESOTALocation MINNEAPOLIS, UNITED STATESPosted 1 Apr 2023Deadline 31 Jan 2028
NIHUS FederalResearch GrantFY2025AffectAntioncogene Protein p53ApoptosisApoptosis PathwayAvian Myelocytomatosis Viral Oncogene HomologBasal Transcription FactorBasal transcription factor genesBody TissuesBreast CancerBreast Epithelial CellsBypassCRISPRCRISPR/Cas systemCancer TreatmentCancersCell BodyCell Communication and SignalingCell Cycle ArrestCell Fate ControlCell Fate RegulationCell FractionCell SignalingCellsCellular OncogeneCellular StressCellular Stress ResponseCellular Tumor Antigen P53Clustered Regularly Interspaced Short Palindromic RepeatsDNA DamageDNA InjuryDNA mutationDataDevelopmentFluorescence Light MicroscopyFluorescence MicroscopyFrequenciesGene Action RegulationGene Down-RegulationGene ExpressionGene Expression MonitoringGene Expression Pattern AnalysisGene Expression ProfilingGene Expression RegulationGene RegulationGene Regulation ProcessGene TranscriptionGeneral Transcription Factor GeneGeneral Transcription FactorsGenesGenetic ChangeGenetic TranscriptionGenetic defectGenetic mutationGenotoxic StressGenotoxinsGoalsHealthHeterogeneityHumanIndividualIntracellular Communication and SignalingMYC Transcription FactorMYC geneMalignant Breast NeoplasmMalignant CellMalignant Neoplasm TherapyMalignant Neoplasm TreatmentMalignant NeoplasmsMalignant TumorMeasurementMediatingMicroscopyModelingModern ManMolecularMutagensMutationNucleic Acid Regulator RegionsNucleic Acid Regulatory SequencesOncoprotein p53OutcomeP53PathologicPathway interactionsPatternPhosphoprotein P53Phosphoprotein pp53PhysiologicPhysiologic pulsePhysiologicalPopulationProgrammed Cell DeathProtein TP53ProteinsProto-Oncogene Products c-mycProto-Oncogene Proteins c-mycProto-OncogenesPublic HealthPulseRNA ExpressionRecoveryRegulationRegulatory RegionsRepressionResearchResistanceRoleSignal PathwaySignal TransductionSignal Transduction SystemsSignalingStimulusStressSystemTP53TP53 geneTRP53TestingTherapeuticTimeTissuesTranscript Expression AnalysesTranscript Expression AnalysisTranscriptionTranscription Factor Proto-OncogeneTranscription RepressionTranscription factor genesTumor CellTumor Protein p53Tumor Protein p53 GeneVariantVariationWorkanalyze gene expressionanti-cancer therapybiological adaptation to stressbiological signal transductionc-ONCc-myc Proteinscancer cellcancer therapycancer-directed therapycell killingcell stresscell transformationchemotherapydevelopmentalgain of functiongene expression analysisgene expression assaygene repressiongenetic regulatory elementgenome editinggenome mutationgenomic editinggenotoxic agentimprovedinnovateinnovationinnovativeinsightmalignancymalignant breast tumormammary epithelial cellsmammary gland epithelial cellsmethod developmentmyc Oncogenesmyc Proto-Oncogene Product p62myc Proto-Oncogene Proteinsneoplasm/cancerneoplastic cellnew therapeutic approachnew therapeutic interventionnew therapeutic strategiesnew therapy approachesnew treatment approachnew treatment strategynovelnovel therapeutic approachnovel therapeutic interventionnovel therapeutic strategiesnovel therapy approachp53 Antigenp53 Genesp53 Tumor Suppressorpathwaypharmacologicpreventpreventingprogramsprotein expressionprotein p53protooncogenereaction; crisisresistantresponsesenescencesenescentsocial rolestress responsestress; reactiontemporal measurementtemporal resolutiontime measurementtranscription factortranscriptional profilingtransformed cellstumor
Description preview
Project Summary
Our long-term goal is to understand how dynamic regulation of signal transduction systems control cellular
stress responses. The focus of this proposal is on identifying the mechanisms by which dynamic
expression of the transcription factors p53 and MYC coordinately regulate apoptosis and senescence in
response to genotoxic stress.…
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