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  • 1990-1994  (2)
  • 1
    Electronic Resource
    Electronic Resource
    Changes of G1 cyclins, cdk2, and cyclin A during the differentiation of HL60 cells induced by TPA (1994)
    Springer
    Molecular and cellular biochemistry 132 (1994), S. 31-37 
    Details
    ISSN: 1573-4919
    Keywords: cell cycle ; TPA ; cyclin ; cdk2 ; differentiation ; acute leukemia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract Differentiation induction by 12-o-tetradecanoyl 13-acetate (TPA) results in the growth arrest of HL60 cells in the G1 phase. However, little is known about the changes of cell cycle-regulating genes during this differentiation process. We investigated the changes of mRNA for various cyclins (A, C, D1, D2, D3 and E) and cdk2. Synchronized HL60 cells began to proliferate immediately after release from cell cycle block and cell cycle synchrony was obvious until the second S phase. TPA-treated cells accumulated in G1 phase within 24 h and most of the cells were arrested in this phase at 36 h. The expression of cyclins and cdk2 was studied by Northern blot hybridization or the reverse-transcription polymerase chain reaction (RT-PCR). TPA treatment altered the expression of all genes studied. The expression of cdk2 and cyclin A mRNA was markedly down-regulated. Cyclin E mRNA expression was also prominently down-regulated from 12 h to 36 h, at which time a second increase of its expression was observed in control cells. In contrast, the expression of cyclin D1 mRNA was induced by TPA, while its expression in control cells was undetectable by Northern blot hybridization throughout the cell cycle. Cyclin C expression was faint and fluctuated irrelevant of cell cycle, but its expression in both control and TPA-treated cells was higher than at baseline. Cyclin D2 expression remained stable in control cells and TPA treatment resulted in slight down-regulation at 12 h, but no difference was observed after 24 h. Cyclin D3 mRNA expression was slightly induced at 6 h, a time when its expression was down-regulated in control cells. At 48 h, these cyclins (C, D2, and D3) showed almost same level of expression as the control. These findings suggest that the down-regulation of cyclin A and cdk2 expression contributes to the G1 arrest of HL60 cells during monocytic differentiation induced by TPA and that cyclin D1 plays an additional role other than the regulation of cell cycle progression.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00925672
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Changes of cell cycle-regulating genes in interferon-treated Daudi cells (1994)
    Springer
    Molecular and cellular biochemistry 136 (1994), S. 117-123 
    Details
    ISSN: 1573-4919
    Keywords: cell cycle ; interferon ; cyclin ; cyclin-dependent kinase ; cdc25 ; weel
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract Interferon (IFN) modulates the expression of several genes and some of themare considered to be responsible for the inhibition of cellular growth. However, the alterations of cell cycle-regulating genes produced by IFN still remain unclear. Accordingly, we studied the expression of cell cycle-regulating genes during IFN-induced growth arrest. Cell cycle synchronized and unsynchronized Daudi Burkitt lymphoma cells were treated with IFN. Both the cell cycle distribution and the expression of cell cycle-regulating genes (cdk2, cdc2, cyclins A, B, C, D3 cdc25, and well) were studied by flow cytometry and by Northern blot hybridization or the reverse-transcription polymerase chain reaction, respectively. Treated cells passed through the first G1 phase and gradually accumulated in the following G1 phase. Expression of cyclins A, B, and D3 oscillated along with the cell cycle progression in control cells, and the alterations of cyclin B expression were especially prominent. Both cdc2 and cdk2 also showed changes, but these were not so distinct as observed with cyclin B. Expression of cdc25 and weel was little affected by cell cycle progression. In IFN-treated cells, expression of cyclins A and B were down-regulated, while that of cyclin C was not. Cyclin D3 expression was also down-regulated at 48 h, followed by an increase at 72 h. Expression of both cdc2 and cdk2 was down-regulated, especially that of the later. Weel expression was down-regulated by IFN but, the expression of cdc25 remained stable. These findings suggest that the modulation of cell cycle-regulating genes, particular by cyclin A and cdk2, plays an important role in IFN-induced cellular growth arrest.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00926071
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    Paper (German National Licenses)
    Fulltext
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