LOCALIZED REVISION OF EPIGENETIC LANDSCAPES INDUCED BY DNA DOUBLE-STRAND BREAKS
M Eugene
Washington Universitycity: Saint Louis country: United States (us)
Grant 5R21ES019779-02 from National Institute Of Environmental Health Sciences
Keywords: Address; Antigen Receptors; ATM Signaling Pathway; base; Binding (Molecular Function); Biological; Biological Process; Cell Culture Techniques; Cell Survival; Cells; Chromatin; chromatin immunoprecipitation; Chromatin Structure; Chromosomal translocation; Chromosome Segregation; Code; Critical Pathways; Custom; Data; Data Set; design; Development; Distal; Distant; DNA; DNA biosynthesis; DNA Damage; DNA Double Strand Break; DNA Repair; DNA Repair Pathway; DNA repair protein; DNA-PKcs; Double Strand Break Repair; Enzymes; Epigenetic Process; epigenomics; Exposure to; Future; Gene Expression; Gene Expression Regulation; Genes; Genetic Transcription; Genome; Genomics; Global Change; Goals; Histone Code; histone modification; Histones; innovation; Ionizing radiation; kappa-Chain Immunoglobulins; Lesion; Liquid substance; Location; Longitudinal Studies; Lymphocyte; Lymphocyte antigen; Malignant Neoplasms; Mammalian Cell; Mammals; Maps; Mediating; Memory; Metabolism; Modification; Molecular; Monitor; Mutagens; novel; Nuclear; Nucleoproteins; Oncogenic; Pathogenesis; Pathway interactions; Pattern; Physiological; Physiological Processes; Pilot Projects; Post-Translational Protein Processing; Process; programs; Proteins; public health relevance; Receptor Gene; Recruitment Activity; Repair Complex; repaired; Research; research study; Resolution; Resources; response; Role; Screening procedure; Signal Transduction; Site; Stimulus; System; Tertiary Protein Structure; Testing; Therapeutic Intervention; Time; Translations; Variant; VDJ Recombinases; Yeasts
Relevance: DNA double-strand breaks (DSBs) are generated upon exposure to genotoxic agents, such as ionizing radiation, and are intermediates during several important physiologic processes, including lymphocyte antigen receptor gene assembly. It is critical that DSBs are appropriately repaired rather than accessing alternative pathways that potentially result in oncogenic chromosomal translocations. We now propose to identify histone modifications that function as intermediates to coordinate the normal repair of DNA-DSBs in mammalian cells
Project start date: 2010-12-01
Project end date: 2012-11-30
Budget start date: 1-DEC-2011
Budget end date: 30-NOV-2012
5R21ES019779-02 (2012): $171000
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