Abstract
Zinc has been discussed to be an inorganic proliferation factor for eukaryotic tissues since about a quarter of a century. It has been found to stimulate DNA synthesis in chick embryo fibroblasts (Rubin and Koide, 1973) and mouse 3T3 fibroblasts (Chesters et al., 1989) and to activate thymidine kinase in various cell types (Prasad, 1979). It has been postulated to act as a second messenger of mitogenesis with baby hamster kidney cells (Grummt et al., 1986). More recently, zinc has been found to be involved in several signal transducing enzymes critical for the induction of mitogenesis in mammalian cells. Zinc stimulated protein kinase C (Zalewski et al., 1990), tyrosine kinase (Vener and Loeb, 1992) and MAP kinase (Hansson et al., 1996), and inhibited a protein phosphatase (Wang et al., 1992). Furthermore, zinc ions have been shown to be required for the onset of differentiation of myoblasts (Petrie et al., 1991). On the genetic level, zinc is an essential constituent of an important class of DNA binding transcription factors possessing zinc finger structures (Berg and Shi, 1996).
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Beyersmann, D., Schmidt, C. (1999). Zinc and Metallothionein in Mammalian Cell Cycle Regulation. In: Sarkar, B. (eds) Metals and Genetics. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-4723-5_10
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DOI: https://doi.org/10.1007/978-1-4615-4723-5_10
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