grant
Project 2: BRCA1-dependent DNA End Resection and Regulation via the 53BP1 Axis
Organization UNIVERSITY OF TEXAS HLTH SCIENCE CENTERLocation SAN ANTONIO, UNITED STATESPosted 1 Sept 2024Deadline 31 Aug 2029
NIHUS FederalResearch GrantFY20253' exonuclease53BP1AbscissionAttenuatedBARD-1BARD1BARD1 geneBRCA deficientBRCA1BRCA1 Associated RING Domain 1 ProteinBRCA1 Gene ProductBRCA1 ProteinBRCA1 geneBRCA1-Associated RING Domain 1BindingBiochemistryBiologicalBiological ChemistryBiophysicsBreast Cancer 1 GeneBreast Cancer 1 Gene ProductBreast Cancer Type 1 Susceptibility GeneBreast Cancer Type 1 Susceptibility ProteinBreast-Ovarian Cancer ProteinCancersCell BodyCell CycleCell Cycle ProgressionCell Division CycleCellsCellular biologyChromatinComplexDNADNA BindingDNA Binding InteractionDNA DamageDNA Damage RepairDNA Double Strand BreakDNA HelicasesDNA InjuryDNA RepairDNA ReplicationDNA SynthesisDNA Unwinding ProteinsDNA annealingDNA biosynthesisDNA boundDNA mutationDNA replication forkDNA unwinding enzymeDeoxyribonucleic AcidDevelopmentDouble Strand Break RepairDouble-Stranded DNADrug resistanceDysfunctionEXO1EXO1 exonucleaseEXO1 geneEarly Onset Gene Breast Cancer 1Early Onset Protein Breast Cancer 1Enzymatic BiochemistryEnzyme GeneEnzymesEnzymologyExcisionExonuclease 1ExtirpationFilamentFirst Gap PhaseFlap EndonucleasesFunctional disorderG1 PhaseG1 periodG2 PhaseG2 periodGap Phase 1Gap Phase 2Genetic ChangeGenetic defectGenetic mutationGenomeGenotoxinsHEX1HEX1 GeneHereditary Breast Cancer 1HumanIonizing Electromagnetic RadiationIonizing radiationLeadLicensingLinkMalignant NeoplasmsMalignant TumorMediatingModern ManMolecular InteractionMutagensMutationNHEJNon-Homologous End JoiningNon-homologous DNA End JoiningNonhomologous DNA End JoiningNonhomologous End JoiningPARP InhibitorPARP-1 inhibitorPARPiPathway interactionsPb elementPhysiopathologyPoly(ADP-ribose) Polymerase InhibitorPoly(ADP-ribose) polymerase 1 inhibitorPredictive Cancer ModelProcessRAD51 proteinRNF53Rad51 recombinaseRadiation-Ionizing TotalReaderRegulationRemovalResearchResistanceResource SharingRoleS PeriodS phaseSecond Gap PhaseSingle-Stranded DNAStressSurgical RemovalSynthesis PeriodSynthesis PhaseTP53BP1TailTherapeuticTumor Suppressor ProteinsUnscheduled DNA Synthesisaccess restrictionsattenuateattenuatesbiologicbiomarker developmentbiophysical foundationbiophysical principlesbiophysical sciencesbrca 1 genecell biologycell typechemotherapeutic agentchemotherapeutic compoundschemotherapeutic drugschemotherapeutic medicationsdevelopmentaldrug resistantds-DNAdsDNAendonucleaseepigenetic gene silencingepigenetic silencinggenome mutationgenome scalegenome-widegenomewidegenotoxic agenthExoIheavy metal Pbheavy metal leadhelicaseindelinjuredinsertion/deletioninsertion/deletion mutationionizing outputmalignancymutantneoplasm/cancernovelnucleasep202p53-binding protein 1p53BP1pathophysiologypathwayphosphodiesterase IIrad2 nuclease family member, homolog of S. cerevisiae exonuclease 1recruitrepairrepairedreplication forkresectionresistance to Drugresistantresistant to Drugresponseresponse to therapyresponse to treatmentrestorationsingle moleculesocial rolespleen exonucleasespleen phosphodiesterasessDNAstructural biologysynergismsynthetic lethal interactionsynthetic lethalitytargeted cancer therapytherapeutic responsetherapy responsetooltreatment responsetreatment responsivenesstumortumor suppressor
Description preview
PROJECT SUMMARY/ABSTRACT
DNA double strand breaks (DSBs) are induced by genotoxic agents such as ionizing radiation, chemotherapeutic
agents, and during encounters of the DNA replication machinery with DNA damage. The two major, mechanistically
distinct DSB repair pathways are non-homologous DNA end joining (NHEJ) and DNA homology-directed repair…
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