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  • Caspases  (1)
  • Cell death  (1)
  • Erythroid cells  (1)
  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Journal of cancer research and clinical oncology 102 (1981), S. 49-55 
    ISSN: 1432-1335
    Keywords: KMOE cells ; Erythroid cells ; Human cell line ; Erythroid differentiation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Three continuous human cell lines, designated KMOE, derived from a patient with acute erythremia (Di Guglielmo's disease) are reported. The cell lines are the cultures of (1) bone marrow cells, (2) peripheral blood cells, and (3) cells from a tumor developed into an athymic nude mouse after transplantation of the cultured bone marrow cells. Cells of all three lines show morphology of immature erythroblast and have i(17q) marker chromosome. They are negative for both Philadelphia chromosome and Epstein-Barr virus nuclear antigen. Although all KMOE cells in suspension culture are benzidine-negative, benzidine-positive cells are found within colonies formed in semi-solid culture media. The relative number of colonies with benzidine-positive cells is increased when sodium butyrate is added to the culture. The KMOE cell lines are human erythroid cell lines with erythroblastic morphology and still retain their tendency for differentiation.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1615-6102
    Keywords: Caspases ; Tumor necrosis factor ; Oligodendrocytes ; Cell death
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Summary Oligodendrocytes are myelin-forming cells in the mammalian central nervous system. About 50% of oligodendrocytes undergo cell death in normal development. In addition, massive oligodendrocyte cell death has been observed in multiple sclerosis. Tumor necrosis factor (TNF) is thought to be one of the mediators responsible for the damage of oligodendrocytes in multiple sclerosis. The addition of TNF-α to primary cultures of oligodendrocytes significantly decreased the number of live cells in 72 h. DNA fragmentation was detected in TNF-treated oligodendrocytes at 36 h by TUNEL assay. Chemical inhibitors Ac-YVAD-CHO (a specific inhibitor of caspase-1 [ICE]-like proteases) as well as Ac-DEVDCHO (a specific inhibitor of caspase-3[CPP32]-like proteases) enhanced the survival of oligodendrocytes treated with TNF-α, indicating that caspase-1- and the caspase-3-mediated cell-death pathways are activated in TNF-induced oligodendrocyte cell death. Caspase-11 is involved in activation of caspase-1. Oligodendrocytes fromCASP-11-deficient mice are partially resistant to TNF-induced oligodendrocyte cell death. Our results suggest that the inhibition of caspases may be a novel approach to treat multiple sclerosis.
    Type of Medium: Electronic Resource
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