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pubmed-article:2770765pubmed:abstractTextDNA damage inflicted by the alkylating agent N-methyl-N'-nitro-N-nitrosoguanidine, or by UV254nm, stimulated the catabolism of protein-bound poly(ADP-ribose) in the chromatin of cultured hepatocytes. The stimulation was highest at the largest doses of DNA-damaging treatment. As a consequence, the half-life of ADP-ribosyl polymers may drop to less than 41 s. This rapid turnover contrasts with the slow catabolism of a constitutive fraction of polymers exhibiting a half-life of 7.7 h. Our data suggest that post-incisional stimulation of poly(ADP-ribose) biosynthesis in DNA-excision repair is coupled with an adaptation of poly(ADP-ribose) catabolism in mammalian cells.lld:pubmed
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pubmed-article:2770765pubmed:articleTitlePoly(ADP-ribose) catabolism in mammalian cells exposed to DNA-damaging agents.lld:pubmed
pubmed-article:2770765pubmed:affiliationUniversity of Zürich-Tierspital, Institute of Pharmacology and Biochemistry, Switzerland.lld:pubmed
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