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  • 1
    Electronic Resource
    Electronic Resource
    Insulin receptor internalization defect in an insulin-resistant mouse melanoma cell line (1989)
    s.l. : American Chemical Society
    Biochemistry 28 (1989), S. 9750-9757 
    Details
    ISSN: 1520-4995
    Source: ACS Legacy Archives
    Topics: Biology , Chemistry and Pharmacology
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1021/bi00451a031
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Growth suppression of hybrids between transformed cells and normal fibroblasts in serum-free medium: Correlation with retention of human chromosomes (1987)
    Springer
    Somatic cell and molecular genetics 13 (1987), S. 587-596 
    Details
    ISSN: 1572-9931
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Somatic cell hybrids formed by crossing PG19 mouse melanoma cells with mouse embryo fibroblasts have a reduced ability to proliferate in growth factor-unsupplemented serum-free medium relative to the parental melanoma cells. The suppression of growth of the hybrid cells in serum-free medium is attributable to a strict requirement of these cells for polypeptide growth factors (insulin plus platelet-derived growth factor, fibroblast growth factor, or epidermal growth factor). In contrast, the parental melanoma cells are able to grow without exogenously added growth factors. Fifteen hybrids derived from crosses between mouse L cells and normal human skin fibroblasts also have been tested for ability to grow in growth factor-unsupplemented serum-free medium. Depending on which human chromosomes are retained, growth of these hybrids in serum-free medium is also suppressed relative to growth of the L cell parent. There appear to be several genes on different chromosomes that are involved in suppression of serum-free growth of the fibroblast × L cell hybrids. One weak suppressor gene appears to be on the human X chromosome.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01534479
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Responsiveness to insulin is a dominant characteristic in somatic cell hybrids (1978)
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Cellular Physiology 97 (1978), S. 189-198 
    Details
    ISSN: 0021-9541
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: The mouse melanoma cell line PG19 has been found to be unresponsive to the growth-stimulatory action of insulin, although it responds well to other growth factors present in serum. Insulin stimulates DNA synthesis in mouse embryo fibroblasts, and responsiveness to insulin has been found to be a dominant characteristic in mouse fibroblast x PG19 hybrids. To examine the possibility that the unresponsiveness to insulin of the melanoma cells is attributable to a lack of insulin receptors, we have measured the binding of 125I-labeled insulin to the fibroblasts, melanoma cells, and fibroblast x melanoma hybrids. Insulin binds to the surface of the melanoma cells; however, the binding affinity appears to be lower than that observed for binding to diploid fibroblasts. In addition, the dissociation of insulin from the melanoma cells is not accelerated by excess unbound insulin, a kinetic effect observed in the dissociation of insulin from the fibroblasts and fibroblast x melanoma hybrids. This suggests that the class of insulin receptors characterized by this effect is absent on the PG19 cells, and present on the fibroblasts and fibroblast x PG19 hybrids.
    Additional Material: 4 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcp.1040970208
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  • 4
    Electronic Resource
    Electronic Resource
    Complementation for the growth response to insulin and MSA occurs at a step distal to hormone-receptor interaction in mouse embryo fibroblast × melanoma cell hybrids (1983)
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Cellular Physiology 114 (1983), S. 123-131 
    Details
    ISSN: 0021-9541
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: The PG19 mouse melanoma cell line does not respond to the mitogenic effects of insulin either in serum-deprived quiescent cultures or when growing in hormone-supplemented serum-free medium, while melanoma × mouse embryo fibroblast hybrids respond under both conditions. It has been proposed that some growth effects of insulin are mediated by its binding to receptors for insulin-like growth factors. To determine whether the PG19 cells do not respond to insulin because they lack receptors for MSA (multiplication-stimulating activity, an insulin-like growth factor produced by BRL-3A cultured rat liver cells), we have examined growth effects and receptor binding of MSA in the melanoma and hybrid cells. MSA stimulates [3H]thymidine incorporation in three melanoma × mouse embryo fibroblast hybrid clones but not in the parental melanoma cells. Thus the pattern of response of the melanoma cells and hybrids to MSA directly parallels their response to insulin. The melanoma cells and hybrids all have high-affinity specific MSA binding sites (KD = 10-27 nM), indicating that the inability of the melanoma cells to respond to MSA is not attributable to a lack of MSA receptors. Insulin competes very poorly for binding of MSA to hybrid clone 7 but is nevertheless able to stimulate [3H]thymidine incorporation in this clone. This strongly suggests that the effects of insulin on [3H]thymidine incorporation in this clone are not mediated by its binding to MSA receptors. Insulin and MSA stimulate protein synthesis and inhibit protein degradation in the hybrids but not in the parental melanoma cells. These results suggest that both insulin and MSA action are blocked in the melanoma cells at a step distal to the binding of either hormone to its cellular receptors but prior to stimulation of protein synthesis.
    Additional Material: 10 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcp.1041140120
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  • 5
    Electronic Resource
    Electronic Resource
    Growth response to insulin in mouse melanoma cells and fibroblast × melanoma hybrids (1980)
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Cellular Physiology 105 (1980), S. 81-92 
    Details
    ISSN: 0021-9541
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: PG19 mouse melanoma cells arrest growth when they become confluent in medium containing low concentrations of serum. Under these conditions, insulin does not stimulate DNA synthesis in the mouse melanoma cells, whereas it does in mouse embryo fibroblats and fibroblast × melanoma hybrids. A detailed examination of the binding of insulin to the melanoma cells and fibroblast × melanoma hybrids in the presence of bacitracin has shown that they have approximately equal numbers of insulin receptors, and that these receptors have similar affinities for insulin. These results indicate that the unresponsiveness of the melanoma cells to the mitogenic action of insulin is not attributable to a lack of insulin receptors. Although insulin does not stimulate incorporation of 3Hthymidine into DNA in confluent cultures of the melanoma cells, it does stimulate uptake of α-aminoisobutyrate, indicating that the insulin receptors are functional and that insulin elicits an acute response in these cells. In hormone-supplemented serum-free medium, insulin does not stimulate growth of the melanoma cells, while it does stimulate growth of the fibroblast × melanoma hybrid. This suggests that an acute response to insulin is not sufficient for stimulation of growth either in confluent growth-arrested cells or in exponentially growing cells in serum-free medium.
    Additional Material: 8 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcp.1041050111
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