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Increased neutrophil respiratory burst in bcr-null mutants.

Cell | Mar 10, 1995

http://www.ncbi.nlm.nih.gov/pubmed/7889565

Philadelphia (Ph)-positive leukemias invariably contain a chromosomal translocation fusing BCR to ABL. The BCR-ABL protein is responsible for leukemogenesis. Here we show that exposure of bcr-null mutant mice to gram-negative endotoxin led to severe septic shock and increased tissue injury by neutrophils. Neutrophils of bcr (-/-) mice showed a pronounced increase in reactive oxygen metabolite production upon activation and were more sensitive to priming stimuli. Activated (-/-) neutrophils displayed a 3-fold increased p21rac2 membrane translocation compared with (+/+) neutrophils. These results connect Bcr in vivo with the regulation of Rac-mediated superoxide production by the NADPH-oxidase system of leukocytes and suggest a link between Bcr function and the cell type affected in Ph-positive leukemia.

Pubmed ID: 7889565 RIS Download

Mesh terms: Actin Cytoskeleton | Animals | Endotoxins | Female | GTP-Binding Proteins | Gene Targeting | Lipopolysaccharides | Male | Mice | Mice, Inbred C57BL | Mutation | Neutropenia | Neutrophil Activation | Neutrophils | Oncogene Proteins | Protein-Tyrosine Kinases | Proto-Oncogene Proteins | Proto-Oncogene Proteins c-bcr | Respiratory Burst | Shock, Septic | Superoxides | Toxemia | rac GTP-Binding Proteins

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Associated grants

  • Agency: NCI NIH HHS, Id: CA50248
  • Agency: NHLBI NIH HHS, Id: HL 48008

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