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- W2054291881 abstract "Abstract Acute BCR-ABL expression during in vitro hematopoietic development of embryonic stem (ES) cells causes expansion of multipotent and myeloid progenitors with a concomitant reduction in differentiation toward erythroblasts. Progenitor cell expansion is due to a rapid, cell autonomous, suppression of programmed cell death with an increase in expression of the antiapoptotic molecule BCL-XL. Other antiapoptotic effectors, including AKT, STAT5, and BCL-2 are not up-regulated by BCR-ABL in this system. In addition, the proapoptotic p38 mitogen–activated protein kinase (MAPK) pathway is suppressed by BCR-ABL expression in ES-derived hematopoietic progenitors. Inhibition of p38 MAPK by the small molecule inhibitor SB203580 expanded ES-derived hematopoietic progenitors by an antiapoptotic mechanism and is sufficient to expand ES-derived hematopoietic progenitors to levels approaching 80% of that seen following BCR-ABL expression. In the cellular context of ES-derived hematopoietic progenitors, BCR-ABL expression expands cells by suppressing programmed cell death with a set of antiapoptotic pathways distinct from those previously reported in continuous cell line studies." @default.
- W2054291881 created "2016-06-24" @default.
- W2054291881 creator A5055588065 @default.
- W2054291881 creator A5075795659 @default.
- W2054291881 creator A5083591281 @default.
- W2054291881 creator A5087708211 @default.
- W2054291881 date "2003-05-15" @default.
- W2054291881 modified "2023-09-30" @default.
- W2054291881 title "Cell context–specific effects of the BCR-ABL oncogene monitored in hematopoietic progenitors" @default.
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- W2054291881 doi "https://doi.org/10.1182/blood-2002-11-3376" @default.
- W2054291881 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/12521991" @default.
- W2054291881 hasPublicationYear "2003" @default.
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