| Pathways that suppress programmed DNA breaks from progressing to chromosomal breaks and translocations. | |
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MedLine Citation:
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PMID: 16934538 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Guarding the genome against internal and external assaults requires the coordinated interaction of multiple cellular networks to sense, respond to, and repair breaks in chromosomal DNA. Both external factors such as ionizing radiation or internal events like oxidative damage can cause DNA double stranded breaks (DSBs). DSBs are also part of the normal lymphocyte developmental program where they are an integral element of the mechanisms that generate a diverse immune repertoire in the context of V(D)J and immunoglobulin heavy chain (IgH) class switch recombination (CSR). DSBs initiate a cascade of cellular events that direct cells to pause and properly repair potentially lethal chromosomal breaks. Errors in the repair of both general and lymphocyte-specific DSBs can lead to oncogenic chromosomal translocations . Here, we review recent advances in understanding factors and protein complexes involved in the response to DNA DSBs with a focus on the B lymphocyte specific process of CSR. |
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Authors:
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Sonia Franco; Frederick W Alt; John P Manis |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review Date: 2006-08-24 |
Journal Detail:
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Title: DNA repair Volume: 5 ISSN: 1568-7864 ISO Abbreviation: DNA Repair (Amst.) Publication Date: 2006 Sep |
Date Detail:
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Created Date: 2006-09-01 Completed Date: 2006-12-11 Revised Date: 2011-11-02 |
Medline Journal Info:
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Nlm Unique ID: 101139138 Medline TA: DNA Repair (Amst) Country: Netherlands |
Other Details:
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Languages: eng Pagination: 1030-41 Citation Subset: IM |
Affiliation:
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Howard Hughes Medical Institute, The Children's Hospital Boston, Department of Genetics, Harvard Medical School, Boston, MA 02115, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Cell Cycle Proteins / genetics Chromosome Breakage* DNA Damage* DNA Repair* DNA-Binding Proteins / genetics Genomic Instability Histones / genetics Homeodomain Proteins / genetics Humans Lymphocytes Lymphoma, B-Cell / genetics Protein-Serine-Threonine Kinases / genetics Translocation, Genetic* Tumor Suppressor Protein p53 / genetics Tumor Suppressor Proteins / genetics |
| Grant Support | |
ID/Acronym/Agency:
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P01AI031541/AI/NIAID NIH HHS; P01CA092615/CA/NCI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Cell Cycle Proteins; 0/DNA-Binding Proteins; 0/H2AX protein, mouse; 0/Histones; 0/Homeodomain Proteins; 0/Tumor Suppressor Protein p53; 0/Tumor Suppressor Proteins; 128559-51-3/RAG-1 protein; EC 2.7.11.1/Protein-Serine-Threonine Kinases; EC 2.7.11.1/ataxia telangiectasia mutated protein |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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