BCR-ABL1 kinase inhibits uracil DNA glycosylase UNG2 to enhance oxidative DNA damage and stimulate genomic instability

Leukemia

Volumn 27, Issue 3, 2013, Pages 629-634

  Slupianek, A ^a   Falinski, R ^a   Znojek, P ^a   Stoklosa, T ^a,b   Flis, S ^a   Doneddu, V ^c   Pytel, D ^a,e   Synowiec, E ^d   Blasiak, J ^d   Bellacosa, A ^c   Skorski, T ^a  

^a TEMPLE UNIVERSITY SCHOOL OF MEDICINE   (United States)

^b MEDICAL UNIVERSITY OF WARSAW   (Poland)

^c TEMPLE UNIVERSITY   (United States)

^d UNIVERSITY OF LODZ   (Poland)

^e UNIVERSITY OF PENNSYLVANIA   (United States)

Author keywords

BCR ABL1; BER; chronic myeloid leukemia; genomic instability; reactive oxygen species

Indexed keywords

BCR ABL PROTEIN; BCR ABL1 PROTEIN; GENOMIC DNA; IMATINIB; REACTIVE OXYGEN METABOLITE; UNCLASSIFIED DRUG; UNG2 PROTEIN; URACIL DNA GLYCOSIDASE;

ANIMAL CELL; ARTICLE; CANCER GROWTH; CANCER RECURRENCE; CD34 SELECTION; CELL POPULATION; CHRONIC MYELOID LEUKEMIA; DNA DAMAGE; DOWN REGULATION; ENZYME ACTIVITY; GENOMIC INSTABILITY; HEMATOPOIETIC CELL; HUMAN; HUMAN CELL; LEUKEMIA CELL; NONHUMAN; POINT MUTATION; PRIORITY JOURNAL; PROTEIN EXPRESSION; PROTEIN FUNCTION;

ANIMALS; BLOTTING, WESTERN; CELL NUCLEUS; COMET ASSAY; DNA DAMAGE; DNA, NEOPLASM; FUSION PROTEINS, BCR-ABL; GENOMIC INSTABILITY; HUMANS; LEUKEMIA, MYELOGENOUS, CHRONIC, BCR-ABL POSITIVE; MICE; MUTAGENESIS; NEOPLASTIC STEM CELLS; POINT MUTATION; POLYMERASE CHAIN REACTION; REACTIVE OXYGEN SPECIES; SODIUM-POTASSIUM-EXCHANGING ATPASE; TUMOR CELLS, CULTURED; URACIL-DNA GLYCOSIDASE;

EID: 84875218884     PISSN: 08876924     EISSN: 14765551     Source Type: Journal    
DOI: 10.1038/leu.2012.294     Document Type: Article

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