Unique acceptors for poly(ADP-ribose) in resting,proliferating and DNA-damaged human lymphocytes |
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Authors: | Carol S. Surowy Nathan A. Berger |
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Affiliation: | 1. The Hematology/Oncology Division of the Department of Medicine, Washington University School of Medicine St. Louis, MO 63110 U.S.A.;2. The Jewish Hospital of St. Louis, 216 South Kingshighway, St. Louis, MO 63110 U.S.A. |
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Abstract: | Acceptor proteins for poly(adenosine diphosphoribosyl)ation were determined in resting human lymphocytes, in lymphocytes with N-methyl-N′-nitro-N-nitrosoguanidine-induced DNA damage and in lymphocytes stimulated to proliferate by phytohemagglutinin. Kinetic studies showed that the increase in ADP-ribosylation which occurred in response to N-methyl-N′-nitro-N-nitrosoguanidine (MNNG) treatment was greater in magnitude but more transient in duration than that which occurred in phytohemagglutinin-stimulated cells. Gel electrophoretic analyses revealed that MNNG treatment and phytohemagglutinin stimulation both caused an increase in ADP-ribosylation of poly(ADP-ribose) polymerase and core histones. In MNNG-treated cells, an increase in ADP-ribosylation of histone H1 was also observed. In contrast, phytohemagglutinin-stimulated cells showed no increase in ADP-ribosylation of histone H1. In MNNG-treated cells there was also ADP-ribosylation of a protein of molecular weight 62 000, while in phytohemagglutinin-stimulated cells there was a marked increase in ADP-ribosylation of a protein of molecular weight 96000. MNNG treatment of phytohemagglutinin-stimulated cells produced a pattern of ADP-ribosylation that appeared to be due to the combined effects of the individual treatments. 3-Aminobenzamide effectively inhibited ADP-ribosylation under all treatment conditions. |
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Keywords: | Poly(ADP - ribose) DNA damage Acceptor protein (Human lymphocyte) Hepes 4-(2-hydroxyethyl)-1-piperazineethanesulfonic acid HMG high-mobility group dimethylsulfoxide MNNG poly(ADP-ribose) poly(adenosine diphosphoribose) |
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