Endogenous ADP ribosylation of high mobility group proteins 1 and 2 and histone H1 following DNA damage in intact cells.
Endogenous ADP ribosylation of nonhistone high-mobility group (HMG) proteins and histone H1 was studied in cultured mouse mammary tumor cells following treatment with N-methyl-N'-nitro-N-nitrosoguanidine (MNNG). MNNG treatment of cells caused a rapid and transient increase in ADP ribosylation of histone H1 and HMG 1 and 2, whereas (ADP-ribose)n on HMG 14 and 17 was not affected. 3-Aminobenzamide, an inhibitor of (ADP-ribose)n synthetase, prevented the increase in ADP ribosylation of histone H1 and HMG 1 and 2. This inhibitor enhanced the cell-killing effect of MNNG, but had no significant effect on the removal of methylated purines. The preferential increase in ADP ribosylation of HMG 1 and 2 and histone H1 may be necessary for cell recovery from DNA damage.
D000246:Adenosine Diphosphate Ribose / Q000378:metabolism*; D000818:Animals; D002460:Cell Line; D055598:Chemical Phenomena; D002621:Chemistry; D004260:DNA Repair; D004273:DNA, Neoplasm / Q000378:metabolism; D004586:Electrophoresis / Q000379:methods; D006609:High Mobility Group Proteins / Q000378:metabolism*; D006657:Histones / Q000378:metabolism*; D008325:Mammary Neoplasms, Experimental / Q000378:metabolism; D008769:Methylnitronitrosoguanidine; D051379:Mice; D008809:Mice, Inbred C3H; D009363:Neoplasm Proteins / Q000378:metabolism; D009702:Nucleoside Diphosphate Sugars / Q000378:metabolism*
D004273:DNA, Neoplasm; D006609:High Mobility Group Proteins; D006657:Histones; D009363:Neoplasm Proteins; D009702:Nucleoside Diphosphate Sugars; D008769:Methylnitronitrosoguanidine; D000246:Adenosine Diphosphate Ribose