Abstract
A number of human myeloid leukemia cell lines have been established which can not only be maintained as immature blast cells in continuous, self-renewing culture but also be induced to undergo maturation toward either the myeloid or monocytic phenotype1). Such cell lines have attracted considerable attention in these days because they provide experimentally accessible model systems with which to define basic mechanisms involved in the regulation of myeloid progenitor cell proliferation and differentiation. The HL60 cell line, originally isolated from a patient with acute promyelocytic leukemia, can be lead to myeloid morphological, functional, and biochemical changes have been observed during DMSO-induced differentiation2). In differentiated HL60 cells, purine nucleotide synthesis decreases3), but there have been some reports demonstrating a drastic change in purine nucleotides pool during differentiation4–6). This seem to the presence of a complicated mechanism involved in differentiation. We used DMSO-treated HL60 cells to investigate the role of salvage and de novo pathway for intracellular purine nucleotide metabolism during proliferation and differentiation.
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© 1989 Plenum Press, New York
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Tsutani, H., Yoshimura, T., Uchida, M., Kamiya, K., Ueda, T., Nakamura, T. (1989). Purine Nucleotide Synthesis during Terminal Differentiation. In: Mikanagi, K., Nishioka, K., Kelley, W.N. (eds) Purine and Pyrimidine Metabolism in Man VI. Advances in Experimental Medicine and Biology, vol 253A. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-5673-8_69
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DOI: https://doi.org/10.1007/978-1-4684-5673-8_69
Publisher Name: Springer, Boston, MA
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