Aranda A, Pascual A, Copp R, Samuels H
Instituto de Investigaciones Biomedicas. CSIC. Fctad de Medicina. Universidad Autonoma, Madrid, Spain.
Biochem Biophys Res Commun. 1988 Jan 15;150(1):323-8. doi: 10.1016/0006-291x(88)90523-2.
Incubation of GH1 cells with cholera toxin for 24 h inhibits [32P]ADP-ribose incorporation into histones and non-histone nuclear proteins by more than 50%. The toxin produces a generalized decrease of incorporation into all protein acceptors and into the poly(ADP-ribosyl)ated components excised from chromatin after micrococcal nuclease digestion. The cellular levels of NAD were also decreased (40 to 80%) after treatment with cholera toxin. The inhibition of poly(ADP-ribosyl)ation is preceded by an increase of [32P]ADP-ribose incorporation, since incubation with the toxin for 3 h caused an increase instead of a decrease of incorporation. Incubation with dibutyryl cyclic AMP for 24 h also inhibited nuclear poly(ADP-ribosyl)ation, thus showing that the effect of cholera toxin might be mediated by cyclic AMP.
将GH1细胞与霍乱毒素孵育24小时，可使[32P]ADP-核糖掺入组蛋白和非组蛋白核蛋白的量减少50%以上。该毒素使掺入所有蛋白质受体以及微球菌核酸酶消化后从染色质中切除的多（ADP-核糖基）化成分的量普遍减少。用霍乱毒素处理后，细胞内NAD水平也降低了（40%至80%）。多（ADP-核糖基）化的抑制之前是[32P]ADP-核糖掺入量的增加，因为与毒素孵育3小时导致掺入量增加而非减少。用二丁酰环磷酸腺苷孵育24小时也抑制了核多（ADP-核糖基）化，因此表明霍乱毒素的作用可能由环磷酸腺苷介导。
