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    Regulation of apoptosis in myeloid cells by interferon consensus sequence-binding protein.

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    Author
    Gabriele, L; Phung, J; Fukumoto, J; Segal, D; Wang, IM; Giannakakou, P; Giese, NA; Ozato, K; Morse, HC
    Date
    1999-08-02
    Source Title
    Journal of Experimental Medicine
    Publisher
    Rockefeller University Press
    University of Melbourne Author/s
    Segal, David
    Affiliation
    Medical Biology (W.E.H.I.)
    Metadata
    Show full item record
    Document Type
    Journal Article
    Citations
    Gabriele, L., Phung, J., Fukumoto, J., Segal, D., Wang, I. M., Giannakakou, P., Giese, N. A., Ozato, K. & Morse, H. C. (1999). Regulation of apoptosis in myeloid cells by interferon consensus sequence-binding protein.. J Exp Med, 190 (3), pp.411-421. https://doi.org/10.1084/jem.190.3.411.
    Access Status
    Open Access
    URI
    http://hdl.handle.net/11343/257219
    DOI
    10.1084/jem.190.3.411
    Open Access at PMC
    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2195590
    Abstract
    Mice with a null mutation of the gene encoding interferon consensus sequence-binding protein (ICSBP) develop a disease with marked expansion of granulocytes and macrophages that frequently progresses to a fatal blast crisis, thus resembling human chronic myelogenous leukemia (CML). One important feature of CML is decreased responsiveness of myeloid cells to apoptotic stimuli. Here we show that myeloid cells from mice deficient in ICSBP exhibit reduced spontaneous apoptosis and a significant decrease in sensitivity to apoptosis induced by DNA damage. In contrast, apoptosis in thymocytes from ICSBP-deficient mice is unaffected. We also show that overexpression of ICSBP in the human U937 monocytic cell line enhances the rate of spontaneous apoptosis and the sensitivity to apoptosis induced by etoposide, lipopolysaccharide plus ATP, or rapamycin. Programmed cell death induced by etoposide was specifically blocked by peptides inhibitory for the caspase-1 or caspase-3 subfamilies of caspases. Studies of proapoptotic genes showed that cells overexpressing ICSBP have enhanced expression of caspase-3 precursor protein. In addition, analyses of antiapoptotic genes showed that overexpression of ICSBP results in decreased expression of Bcl-X(L). These data suggest that ICSBP modulates survival of myeloid cells by regulating expression of apoptosis-related genes.

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