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Volumn 36, Issue 1, 2015, Pages 13-24
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Enhanced non-homologous end joining contributes toward synthetic lethality of pathological RAD51C mutants with poly (ADP-ribose) polymerase
a a a a |
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Author keywords
[No Author keywords available]
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Indexed keywords
CHROMATIN;
DNA BINDING PROTEIN;
ENZYME INHIBITOR;
NICOTINAMIDE ADENINE DINUCLEOTIDE ADENOSINE DIPHOSPHATE RIBOSYLTRANSFERASE;
RAD51C PROTEIN, HUMAN;
ANTAGONISTS AND INHIBITORS;
BREAST TUMOR;
CELL CYCLE;
CELL PROLIFERATION;
CHROMATIN;
CHROMOSOME ABERRATION;
DNA DAMAGE;
DNA END JOINING REPAIR;
ENZYMOLOGY;
FEMALE;
FLUORESCENT ANTIBODY TECHNIQUE;
GENETIC RECOMBINATION;
GENETICS;
GENOMIC INSTABILITY;
HELA CELL LINE;
HUMAN;
METABOLISM;
MUTATION;
PATHOLOGY;
TUMOR CELL CULTURE;
WESTERN BLOTTING;
BLOTTING, WESTERN;
BREAST NEOPLASMS;
CELL CYCLE;
CELL PROLIFERATION;
CHROMATIN;
CHROMOSOME ABERRATIONS;
DNA DAMAGE;
DNA END-JOINING REPAIR;
DNA-BINDING PROTEINS;
ENZYME INHIBITORS;
FEMALE;
FLUORESCENT ANTIBODY TECHNIQUE;
GENOMIC INSTABILITY;
HELA CELLS;
HUMANS;
MUTATION;
POLY(ADP-RIBOSE) POLYMERASES;
RECOMBINATION, GENETIC;
TUMOR CELLS, CULTURED;
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EID: 84925021159
PISSN: None
EISSN: 14602180
Source Type: Journal
DOI: 10.1093/carcin/bgu211 Document Type: Article |
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Times cited : (30)
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References (0)
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