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  • 1
    Electronic Resource
    Electronic Resource
    Apoptosis during HL-60 cell differentiation is closely related to a G0/G1 cell cycle arrest (1995)
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Cellular Physiology 164 (1995), S. 74-84 
    Details
    ISSN: 0021-9541
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: The cell cycle-associated differences in the susceptibility to apoptosis were examined in HL-60 cells before and after differentiation with phorbol 12, 13-dibutyrate (PDBu). HL-60 cells in various phases of the cell cycle were separated by the counterflow centrifugal elutriation and the susceptibility to apoptosis was measured by the morphological examination and by DNA fragmentation assay. Undifferentiated HL-60 cells in S phase showed a significantly higher susceptibility to apoptosis than those in G0/G1 or G2/M phase either in the absence or presence of apoptosis-inducing reagents such as A23187, actinomycin D (Act D), and cycloheximide (CHX). In contrast, PDBu-treated HL-60 cells preferentially underwent apoptosis in G0/G1 phase. When untreated HL-60 cells enriched for G0/G1 phase were recultured in a complete medium, the percentage of apoptotic cells increased after 6-12 h in correlation with the increase in S-phase cells. When the same experiment was performed with PBDu-treated cells, spontaneous increase of apoptotic cells was observed while almost all cells remained in G0/G1 phase. Northern blot analysis revealed that undifferentiated cells expressed the same amounts of bcl-2 mRNA in each cell cycle phase, whereas G0/G1-predominant reduction of bcl-2 mRNA was noted in PDBu-treated cells. There was no difference in the amounts of CD11b mRNA between G0/G1 fraction and S + G2/M fraction of differentiated HL-60 cells. BCL-2 overexpression could almost completely abrogate the G0/G1-predominant induction of apoptosis in differentiated HL-60 cells. These results suggest that G0/G1 cell cycle arrest and down-regulation of bcl-2 mRNA in G0/G1 phase might be associated with apoptosis in differentiated HL-60 cells whereas the weakness of chromatin structure in S phase might be related to apoptosis in undifferentiated HL-60 cells. © 1995 Wiley-Liss, Inc.
    Additional Material: 9 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcp.1041640110
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  • 2
    Electronic Resource
    Electronic Resource
    Tenascin-C induction by the diffusible factor epidermal growth factor in stromal-epithelial interactions (1995)
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Cellular Physiology 165 (1995), S. 18-29 
    Details
    ISSN: 0021-9541
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: Tenascin-C, a six-armed extracellular matrix glycoprotein, is expressed in a temporally and spatially restricted pattern during carcinogenesis and invasion or metastasis of carcinoma cells in association with stromal-epithelial interactions. The human epidermoid carcinoma-derived cell lines, A431 and HEp-2, which do not express tenascin-C by themselves in vitro, do express tenascin-C after transplantation into nude mice, and transforming growth factor β1 (TGF-β1) induces them to express tenascin-C in vitro. Epidermal growth factor (EGF) induced tenascin-C in these cells more effectively (about 3.5-fold greater) than did TGF-β1. Hepatocyte growth factor (HGF) and platelet-derived growth factor (PDGF) had little effect on the induction of tenascin-C. EGF also induced other extracellular matrix components, fibronectin and laminin. Tenascin-C was also induced when the carcinoma cells were co-cultured with embryonic fibroblasts from mice which were homozygous for a null mutation in the tenascin-C gene, or when the conditioned medium from these cells was added. The induction of tenascin-C in the co-culture was reduced by treating the cells with antibodies against EGF or its receptor. The addition of EGF caused both cell types to disrupt their cytoskeleton and focal contacts as evidenced by the loss of stress fibers and vinculin plaques. EGF did neither induce tenascin-C nor affect the morphology in tenascin-C-nonproducing A549 carcinoma cells, which did not produce tenascin-C after transplantation. Thus, EGF induces tenascin-C in tenascin-C-nonproducing human carcinoma cells through EGF receptors. Furthermore, in stromalepithelial interactions, the diffusible factor EGF participates in the induction of human tenascin-C in these cells through EGF receptors. © 1995 Wiley-Liss Inc.
    Additional Material: 8 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcp.1041650104
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  • 3
    Electronic Resource
    Electronic Resource
    Development of androgenetic mouse embryos produced by in vitro fertilization of enucleated oocytes (1993)
    New York, NY [u.a.] : Wiley-Blackwell
    Molecular Reproduction and Development 34 (1993), S. 43-46 
    Details
    ISSN: 1040-452X
    Keywords: Androgenetic eggs ; Enucleation ; Mouse oocytes ; In vitro fertilization ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology
    Notes: Enucleated mouse oocytes were successfully fertilized in vitro, and the resultant androgenetic eggs developed to the blastocyst stage. The proportion of enucleated oocytes fertilized in vitro was high (87-99%) at sperm concentrations ranging from 10-100 × 104/ml. At high sperm concentrations (100-1,000 × 104), 35-45% of the fertilized eggs resulted in heterozygous bispermic androgenones. The proportion of hemizygous haploid and heterozygous diploid androgenones developing to blastocysts was 11% and 43%, respectively. Hemizygous diploidization, however, showed no positive effect on development. These results clearly show that the procedure reported here is efficient and reliable for the production of androgenetic eggs. © 1993 Wiley-Liss, Inc.
    Additional Material: 3 Tab.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/mrd.1080340107
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  • 4
    Electronic Resource
    Electronic Resource
    Treatment of myeloid leukemic cells with the phosphatase inhibitor okadaic acid induces cell cycle arrest at either G1/S or G2/M depending on dose (1992)
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Cellular Physiology 150 (1992), S. 484-492 
    Details
    ISSN: 0021-9541
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: The phosphatase inhibitor okadaic acid was found to induce cell cycle arrest of human myeloid leukemic cell lines HL-60 and U937 in a concentration- and time-dependent manner. Exposure to low concentrations of okadaic acid (2-8nM) for 24-48 hr caused 〉70% of cells to arrest at G2/M, with up to 40% of the cells arrested in early mitosis. Cell viability decreased rapidly after 48 hr of treatment, and morphological and DNA structure analysis indicated that this was primarily due to the induction of apoptosis. The cells arrested in mitosis by 8 nM okadaic acid could be highly enriched by density gradient centrifugation and underwent apoptosis when further cultured either with or without okadaic acid, indicating that the effects of okadaic acid were irreversible. In contrast to the effects of low concentrations of okadaic acid, high concentrations (500 nM), inhibited proliferation in less than 3 hr. Remarkably, the majority of cells also entered a mitosis-like state characterized by dissolution of the nuclear membrane and condensation and partial separation of chromosomes. However, these cells had a diploid content of DNA, indicating that the cell cycle arrest occurred at G1/S with premature chromosome condensation (PCC), rather than at G2/M. If cells were first blocked at G1/S with hydroxyurea and then treated with okadaic acid, 〉90% developed PCC in less than 3 hr without replicating their DNA. Caffeine was not able to induce PCC in these cells, either with or without prior inhibition of DNA synthesis. These results provide further evidence that an interacting system of cell cycle associated phosphatases and kinases control the initiation of each phase of the cell cycle in higher eukaryotes and further suggest that okadaic acid will be useful in manipulating the cell cycle of leukemic cells.
    Additional Material: 7 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcp.1041500308
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