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  • 1
    Electronic Resource
    Electronic Resource
    CHARACTERIZATION OF RETINOIC ACID-INDUCED ALTERATIONS IN THE PROLIFERATION AND DIFFERENTIATION OF A MURINE AND A HUMAN MELANOMA CELL LINE IN CULTURE (1981)
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 359 (1981), S. 0 
    Details
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1749-6632.1981.tb12744.x
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  • 2
    Electronic Resource
    Electronic Resource
    Expression of galectins on microvessel endothelial cells and their involvement in tumour cell adhesion (1994)
    Springer
    Glycoconjugate journal 11 (1994), S. 462-468 
    Details
    ISSN: 1573-4986
    Keywords: galectin ; lectin ; cell adhesion ; endothelial cell ; metastasis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology
    Notes: Abstract Lactoside-binding lectins (galectins) with molecular weights of about 14.5 kDa (galectin-1) and 29–35 kDa (galectin-3) bind preferentially to polylactosaminoglycan-containing glycoconjugates and have been found on the surface of tumour cells and implicated in cell-cell and cell-extracellular matrix adhesion and metastasis. We have demonstrated by immunoblotting that both galectin-1 and galectin-3 are present in extracts of endothelial cells cultured from bovine aorta, rat lung, mouse lung and mouse brain microvessels, whereas mouse hepatic sinusoidal endothelial cells expressed primarily galectin-1. These galectins were also localized by indirect immunofluorescent labelling on the surface of the different endothelial cells in culture and by immunohistochemical staining in human tissuesin vivo. Anti-galectin-1 antibodies inhibited the adhesion of liver-preferring murine RAW117-H10 large-cell lymphoma cells to hepatic sinusoidal endothelial cells or lung microvessel endothelial cellsin vitro. The data indicate that galectin-1 is expressed on the extracellular surface of endothelial cells and can mediate in part the adhesion of RAW117-H10 cells to liver microvessel endothelial cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00731282
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  • 3
    Electronic Resource
    Electronic Resource
    Inhibition of proliferation and induction of apoptosis in cervical carcinoma cells by retinoids: Implications for chemoprevention (1995)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 59 (1995), S. 80-86 
    Details
    ISSN: 0730-2312
    Keywords: Apoptosis ; cervical cancer ; chemoprevention ; N-(4-hydroxyphenyl)retinamide ; retinoids ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: The effects of retinoids including all-trans-retinoic acid (ATRA), 13-cis-retinoic acid (13CRA), and N-(4-hydroxyphenyl)retinamide (4-HPR) on several cervical carcinoma cell lines in culture were investigated as a prelude to investigating the mechanisms underlying the chemopreventive potential of retinoids in cervical cancer. We found that when used at a concentration of 1 μM, 13CRA and ATRA inhibited the proliferation of three cell lines (ME-180 [HPV 68], SiHa [HPV 18], and HT-3 [HPV-]) by about 80% after a seven-day treatment. Three other cell lines (MS-751 [HPV 18], HeLa [HPV 18], C-33A [HPV-]) were moderately inhibited (30-48%), and two (C-4 II [HPV 18], CaSki [HPV 16]) responded poorly (〈 25% inhibition). 4-HPR failed to inhibt the growth of any of these cell lines when used at 1 μM; however, when used at 5 or 10 μM, it induced apoptosis as evidenced DNA fragmentation in several of the cell lines and was more potent in this effect than 10 μM ATRA. Retinoids that induce apoptosis in malignant cells may be able to exert similar effects on premalignant cells. Such retinoids would be expected to exhibit greater potency as chemopreventive agents than retinoids that exert only cytostatic effects.
    Additional Material: 2 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcb.240590911
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  • 4
    Electronic Resource
    Electronic Resource
    Enhancement of melanotic expression in cultured mouse smelanoma cells by retinoids (1981)
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Cellular Physiology 106 (1981), S. 179-189 
    Details
    ISSN: 0021-9541
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: Retinoic acid (RA), which reduces the rate of cell proliferation in S91 mouse melanoma clone C2 cells, was found to stimulate the expression of their melanotic phenotype. RA treatment also induced the extension of long cellular processes. The RA effects on melanogenesis included stimulation of tyrosinase activity and augmentation of cellular melanin content to levels 3- to 4-fold higher than in untreated cultures at similar cell densities. These effects became apparent after 48 hours of exposure to 10-5 M RA and increased thereafter. Halfmaximal stimulation in cells treated for 6 days occurred at 5 × 10-7 M RA. Although the degrees of melanogenesis enhancement by RA (10-5 M) and by α-melanocyte stimulatory hormone (2 × 10-7 M) were similar, the former did not alter the intracellular cAMP level, whereas the latter induced a transient 4-fold increase. In high-passage (p28) cells, as well as in low-passage cells (〈 p10) treated with tyrosinase inhibitor phenylthiocarbamate, melanin synthesis was suppressed in the absence and presence of RA, yet the ability of RA to inhibit cell proliferation was not compromised. In the presence of the tumor promotor phorbol myristate acetate (〉 5 × 10-9 M) melanin synthesis in control as well as in cells exposed to RA was dramatically inhibited. Phorbol which is not active in tumor promotion had no effect on melanogenesis. In addition to RA, other retinoids, such as 13-cis-retinoic acid, retinyl acetate, the TMMP analog of RA and the phenyl analog of RA, but not the pyridyl analog of RA or retinyl palmitate, also inhibited cell growth and enhanced melanin synthesis.
    Additional Material: 4 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcp.1041060203
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