Sensing and repairing DNA double-strand breaks.
By Stephen P. Jackson. Carcinogenesis, 2002
1,205 citations recorded by the source corpus.
Subfields: Molecular Biology, Oncology, Public Health, Environmental and Occupational Health
View Paper: https://www.semanticscholar.org/paper/4cb46a6369f21193a58886c4326731d5b537b70b
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In Molecular Biology
- J. Bartek
- Lei S. Qi
- M. Löbrich
- P. Jeggo
- Luke A. Gilbert
- Jonathan S. Weissman
- Ines Krüger
- L. Thompson
In Oncology
In Public Health, Environmental and Occupational Health
Citations in the corpus
- Pathways of DNA Double-Strand Break Repair during the Mammalian Cell Cycle (2003, background): “This similarity provides further evidence that each -H2AX focus directly reflects the presence of a DSB. V3 cells complemented with a yeast artificial chromosome containing either the human (V3-147) (6) or the mouse (V3-155) (39) DNA-PKcs gene show a repair capacity similar to that of parental AA8 c”
- DNA damage and its links to neurodegeneration (2014, neutral): “When compared to other lesions, DNA DSBs are rare events; however, DSBs are also extremely deleterious because they can cause large chromosome rearrangements that can either lead to cell death, or promote tumorigenesis (Jackson, 2002).”
- Genome-Scale CRISPR-Mediated Control of Gene Repression and Activation (2014, background): “Additionally, double-stranded DNA breaks can be cytotoxic (Huang et al., 1996; Jackson, 2002).”
- Cellular Stress Responses: Cell Survival and Cell Death (2010, background): “The former constitutes the predominant DNA repair pathway in humans and involves DNA repair proteins such as DNA-PK, Ku70, and Ku80 [181, 182].”
- Unraveling V(D)J Recombination: Insights into Gene Regulation (2004, neutral): “In mice, deficiency for any of the six known NHEJ pro-logs in yeast, while the DNA-dependent protein kinase catalytic subunit (DNA-PKcs) and Artemis evolved more teins, similar to RAG deficiency, results in a SCID phenotype due to inability to join RAG-cleaved V, D, and Jrecently (Jackson, 2002).”
- The role of double-strand break repair — insights from human genetics (2006, background): “DSB response mechanisms DDR pathways encompass processes of DNA-repair and signal-transduction mechanisms that alert the cell to the presence of DNA damage and coordinate the appropriate respons”
- ATM and related protein kinases: safeguarding genome integrity (2003, background): “This is especially true for the response to highly cytotoxic DNA lesions, such as double-strand breaks (DSBs”
- The cell-cycle checkpoint kinase Chk1 is required for mammalian homologous recombination repair (2005, background): “S1 ) proficient in HRR but deficient in the non-homologous end joining pathway (NHEJ), an alternative but more error-prone mechanism of DSB repai”