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Tumor Promoter Phorbol-Myristate-Acetate Induces a Prooxidant State which Causes the Accumulation of Poly(ADP-Ribose) in Fibroblasts

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ADP-Ribosylation of Proteins

Part of the book series: Proceedings in Life Sciences ((LIFE SCIENCES))

Abstract

Many tumor promoters induce a cellular prooxidant state, i.e., they increase the concentrations of active oxygen, organic-hydroperoxides, and -radicals [1]. The question arises, therefore, whether these highly reactive metabolic intermediates play a role in the promotor-induced modulation of the expression of growth- and differentiation-related genes. Posttranslational modification of chromosomal proteins by poly(ADPR) could be involved in this process because it is intimately related to the cellular redox-state, DNA strand breakage, and chromatin conformation. Poly(ADPR) appears to play a role in various aspects of chromatin metabolism. Its inhibition has been shown to affect DNA repair [2, 3], the formation of sister chromatid exchanges and chromosomal aberrations, cell differentiation [4, 5], and malignant transformation [6, 7]. We report our studies of the effect of the mouse skin tumor promoter phorbol-12-myristate-13-acetate (PMA) in cultured rodent and human fibroblasts.

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© 1985 Springer-Verlag Berlin Heidelberg

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Singh, N., Poirier, G.G., Cerutti, P.A. (1985). Tumor Promoter Phorbol-Myristate-Acetate Induces a Prooxidant State which Causes the Accumulation of Poly(ADP-Ribose) in Fibroblasts. In: Althaus, F.R., Hilz, H., Shall, S. (eds) ADP-Ribosylation of Proteins. Proceedings in Life Sciences. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-70589-2_40

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  • DOI: https://doi.org/10.1007/978-3-642-70589-2_40

  • Publisher Name: Springer, Berlin, Heidelberg

  • Print ISBN: 978-3-642-70591-5

  • Online ISBN: 978-3-642-70589-2

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