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  • Articles  (3)
  • EARTH RESOURCES AND REMOTE SENSING
  • Life and Medical Sciences
  • Chemistry and Pharmacology  (3)
  • 1
    Electronic Resource
    Electronic Resource
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 39 (1989), S. 139-151 
    ISSN: 0730-2312
    Keywords: calcium ; Fura-2 ; growth factors ; competence ; PDGF ; autoradiography ; digital image analysis ; FGF ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Although increased free intracellular calcium (Cai) may be one of the main regulators of cell growth and differentiation, studies in cell populations have implied that not all growth factors produce Cai increases. In order to examine in more detail whether Cai increases were related to mitogenesis, we used digital image analysis of intracellular Fura-2 fluorescence to measure Cai in individual BALB/c 3T3 cells stimulated with either platelet-derived growth factor (PDGF) or fibroblast growth factor (FGF). We found that PDGF induced larger and more prolonged Cai increases than FGF did, but that both growth factors induced an initial rapid increase in Cai (〈 2 min) followed by a later sustained increase (〉 20 min). Only the prolonged Cai increase required extracellular calcium. Following PDGF treatment (1-8 units/ml), the percentage of cells with a large peak Cai increase (〉 twofold) correlated with the percentage of cells made competent (subsequent growth in 1% platelet-poor-plasma). In contrast, purified bovine basic FGF (200-800 pg/ml) and recombinant human acidic FGF (10-300 ng/ml) produced peak Cai increases that were not directly correlated with mitogenesis. In addition, concentrations of intracellular Quin 2 that inhibited Cai transients also inhibited PDGF stimulation but not FGF stimulation of mitogenesis. Thus, Cai increases are necessary for mitogenesis in BALB/c 3T3 cells stimulated by PDGF, but not that stimulated by FGF.
    Additional Material: 7 Ill.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 56 (1994), S. 469-479 
    ISSN: 0730-2312
    Keywords: inducible v-sis (PDGF-B) ; signal transduction ; Egr-1 protein ; mutant Ras ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: The early growth response gene, Egr-1, is up-regulated transiently by mitogens and many other simuli in all cells tested. Using NIH3T3 cells conditionally expressing v-sis from a metallothionein promoter, we show that the addition of Zn2+ stimulates the production of PDGF-B(v-sis) and elicits the expression of Egr-1 in a dose-dependent and time-regulated manner. The signal is likely independent of protein kinase C, but depends on tyrosine kinase and other kinase activities and is mediated by c-Ha-Ras since the presence of dominant-negative mutants of Ras and Raf abrogates the induction of Egr-1 expression by Zn2+. Transiently activated Ras expression in NIH3T3 cells also stimulates the transient expression of Egr-1, but cells that constitutively express Rass do not have elevated levels of Egr-1. Transient assays also demonstrated that Zn2+ or activated Ras expression stimulated the activity of a 950 bp Egr-1 promoter-reporter gene construct and this is abrogated in the presence of mutant Ras and Raf. The accumulated data show that Egr-1 gene expression is regulated by multiple mechanisms, as would be needed for putative role in Cell proliferation, in suppression of transformation and in differentiation.
    Additional Material: 9 Ill.
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  • 3
    ISSN: 0730-2312
    Keywords: avian embryo ; peripheral nervous system ; neural crest ; cell-adhesion ; cell migration ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: The peripheral nervous system derives mainly from the neural crest both in the head and trunk. Using markers such as fibronectin (FN), neural cell-adhesion molecule (NCAM), the nuclcolar marker for quail cells in chimaeric embryos, and NC-1, a monoclonal antibody specific to crest cells and their neural derivatives, we have attempted to reconstruct the processes that lead to the formation of peripheral ganglia. Our observations allow us to propose a model of the formation of ganglia based on morphogenetic movements and on variations of crest cell adhesiveness. In most cases, crest cells migrate in morphologically defined and transient pathways that lead them to their final site of arrest; these pathways are always associated with FN, which appears necessary for crest cell attachment and movement in vitro. The directionality of crest cell migration is probably dictated by the cells' motile properties and population pressure in restricted areas suitable for cell movement. The disappearance of the pathways and of the substrate necessary for migration while the population is rapidly dividing may be responsible for the aggregation of crest cells in the case of the sensory ganglia. To the contrary, the aggregation of crest cells into autonomic ganglia (sympathetic, enteric, aid ciliary ganglia) does not seem to obey the same rules, no disappearance of the substratum or of the pathways being obvious; rather, their formation seems correlated with the de novo synthesis of adhesive molecules such as NCAM.
    Additional Material: 6 Ill.
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