Tao Y, Howlett A, Klein C
E.A. Doisy Department of Biochemistry and Molecular Biology, St. Louis University School of Medicine, MO 63104.
Proc Natl Acad Sci U S A. 1992 Jul 1;89(13):5902-6. doi: 10.1073/pnas.89.13.5902.
Nitric oxide-releasing compounds were shown to activate an ADP-ribosyltransferase activity in the cytosol of Dictyostelium discoideum. The enzyme ADP-ribosylated a cytosolic protein of approximately 41 kDa, p41. Neither cGMP nor GTP and its analogues affected this ADP-ribosylation. p41 differs from other substrates ADP-ribosylated by cholera, pertussis, or diphtheria toxins. Treatment of ADP-ribosylated p41 with snake venom phosphodiesterase released adenosine 5'-monophosphate, indicating a mono-ADP-ribose-protein linkage. This linkage was stable to neutral hydroxylamine but was sensitive to mercury ions and iodomethane, suggesting an attachment to a cysteine residue. Treatment of intact cells with nitric oxide-releasing compounds appeared to stimulate the ADP-ribosylation of p41 and this modification was reversible.
已证明释放一氧化氮的化合物可激活盘基网柄菌胞质溶胶中的一种 ADP-核糖基转移酶活性。该酶将一种约 41 kDa 的胞质蛋白(p41)进行 ADP-核糖基化。cGMP、GTP 及其类似物均不影响这种 ADP-核糖基化。p41 与霍乱毒素、百日咳毒素或白喉毒素进行 ADP-核糖基化的其他底物不同。用蛇毒磷酸二酯酶处理 ADP-核糖基化的 p41 可释放 5'-单磷酸腺苷,表明存在单 ADP-核糖-蛋白质连接。这种连接对中性羟胺稳定,但对汞离子和碘甲烷敏感,提示其与半胱氨酸残基相连。用释放一氧化氮的化合物处理完整细胞似乎可刺激 p41 的 ADP-核糖基化,且这种修饰是可逆的。