Modernizing the Nonhomologous End-Joining Repertoire: Alternative and Classical NHEJ Share the Stage
Autor: | Ludovic Deriano, David Roth |
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Přispěvatelé: | Développement lymphocytaire et Oncogénèse, Institut Pasteur [Paris] (IP)-Centre National de la Recherche Scientifique (CNRS), University of Pennsylvania, Institut Pasteur [Paris]-Centre National de la Recherche Scientifique (CNRS), University of Pennsylvania [Philadelphia] |
Jazyk: | angličtina |
Rok vydání: | 2013 |
Předmět: |
Genome instability
MESH: Cell Death DNA End-Joining Repair MESH: V(D)J Recombination MESH: DNA Breaks Double-Stranded Ataxia Telangiectasia Mutated Proteins DNA-Activated Protein Kinase Cell Transformation Genome Double-Stranded 0302 clinical medicine Models DNA Breaks Double-Stranded MESH: Animals MESH: Models Genetic Homologous Recombination MESH: Ataxia Telangiectasia Mutated Proteins VDJ Recombinases DNA End-Joining Repair/*genetics MESH: Mutagenesis Genetics Gene Rearrangement 0303 health sciences MESH: VDJ Recombinases Cell Death MESH: Genomic Instability V(D)J recombination Non-homologous end joining Cell Transformation Neoplastic 030220 oncology & carcinogenesis MESH: Immunoglobulin Class Switching [SDV.IMM]Life Sciences [q-bio]/Immunology DNA damage MESH: Gene Rearrangement Computational biology Biology VDJ Recombinases/physiology Genomic Instability MESH: Homologous Recombination 03 medical and health sciences Ataxia Telangiectasia Mutated Proteins/genetics/physiology Genetic Animals 030304 developmental biology MESH: Genetic Therapy Immunoglobulin Class Switching/genetics Neoplastic Models Genetic Mutagenesis fungi DNA Breaks Gene rearrangement Genetic Therapy MESH: DNA End-Joining Repair Immunoglobulin Class Switching V(D)J Recombination enzymes and coenzymes (carbohydrates) DNA-Activated Protein Kinase/physiology MESH: Cell Transformation Neoplastic Homologous Recombination/genetics MESH: DNA-Activated Protein Kinase Homologous recombination |
Zdroj: | Annual Review of Genetics Annual Review of Genetics, 2013, 47 (1), pp.433-55. ⟨10.1146/annurev-genet-110711-155540⟩ Annual Review of Genetics, Annual Reviews, 2013, 47 (1), pp.433-55. ⟨10.1146/annurev-genet-110711-155540⟩ |
ISSN: | 0066-4197 |
DOI: | 10.1146/annurev-genet-110711-155540 |
Popis: | International audience; DNA double-strand breaks (DSBs) are common lesions that continually threaten genomic integrity. Failure to repair a DSB has deleterious consequences, including cell death. Misrepair is also fraught with danger, especially inappropriate end-joining events, which commonly underlie oncogenic transformation and can scramble the genome. Canonically, cells employ two basic mechanisms to repair DSBs: homologous recombination (HR) and the classical nonhomologous end-joining pathway (cNHEJ). More recent experiments identified a highly error-prone NHEJ pathway, termed alternative NHEJ (aNHEJ), which operates in both cNHEJ-proficient and cNHEJ-deficient cells. aNHEJ is now recognized to catalyze many genome rearrangements, some leading to oncogenic transformation. Here, we review the mechanisms of cNHEJ and aNHEJ, their interconnections with the DNA damage response (DDR), and the mechanisms used to determine which of the three DSB repair pathways is used to heal a particular DSB. We briefly review recent clinical applications involving NHEJ and NHEJ inhibitors. |
Databáze: | OpenAIRE |
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