NAD+-dependent ADP-ribosylation of T Lymphocyte Alloantigen RT6.1 Reversibly Proceeding in Intact Rat Lymphocytes (*)
NAD+-dependent ADP-ribosylation of T Lymphocyte Alloantigen RT6.1 Reversibly Proceeding in Intact Rat Lymphocytes (*)
复制标题
T 淋巴细胞同种抗原 RT6.1 的 NAD 依赖性 ADP 核糖基化在完整大鼠淋巴细胞中可逆进行 (*)
DOI：
10.1074/jbc.270.39.22747
复制
发表时间：
1995
期刊：
影响因子：
--
通讯作者：
T. Katada
中科院分区：
文献类型：
--
作者：
T. Maehama;H. Nishina;S. Hoshino;Y. Kanaho;T. Katada
大鼠T淋巴细胞同种异体抗原6.1(RT6.1)是在大肠杆菌中合成的与麦芽糖结合蛋白融合的蛋白，除具有NAD糖水解酶活性外，还具有NAD依赖的自身ADP核糖化作用。从大鼠组织中分离的淋巴细胞中也观察到RT6.1的这种ADP-核糖化。当表达RT6.1mRNA的完整大鼠淋巴细胞与[α-P]NAD孵育时，其放射性被结合到一个M为31,000的细胞表面蛋白中。用磷脂酰肌醇特异性磷脂酶C处理细胞，并用抗RT6.1抗血清进行免疫沉淀，从细胞表面释放标记的31 kDa蛋白。与蛇毒磷酸二酯酶孵育后，结合到31 kDa蛋白中的放射性被恢复为5‘-[P]AMP，并被NHOH处理去除。这些结果表明，31 kDa蛋白的NAD依赖的修饰是由于糖基磷脂酰肌醇锚定的RT6.1在精氨酸残基上的ADP核糖基化。当RT6.1曾经被[P]ADP-核糖化修饰的完整淋巴细胞在没有NAD的情况下进一步孵育时，[P]ADP-核糖化的RT6.1的放射性降低。降低的放射性以[P]ADP-核糖的形式从孵育液中恢复。在反应混合物中加入ADP-核糖可以有效地抑制这种还原反应。此外，NAD的重现再次引起RT6.1的ADP核糖化。因此，RT6.1的ADP核糖化似乎在完整的大鼠淋巴细胞中可逆地进行。
Rat T lymphocyte alloantigen 6.1 (RT6.1), which was synthesized as the fusion protein with a maltose-binding protein in Escherichia coli, displayed NAD-dependent auto-ADP-ribosylation in addition to an enzyme activity of NAD glycohydrolase. Such ADP-ribosylation of RT6.1 was also observed in lymphocytes isolated from rat tissues as follows. When intact rat lymphocytes expressing RT6.1 mRNA were incubated with [α-P]NAD, its radioactivity was incorporated into a cell surface protein with the M of 31,000. The radiolabeled 31-kDa protein was released from the cell surface by treatment of the cells with phosphatidylinositol-specific phospholipase C and immunoprecipitated with anti-RT6.1 antiserum. The radioactivity incorporated into the 31-kDa protein was recovered as 5′-[P]AMP upon incubation with snake venom phosphodiesterase and also removed by NHOH treatment. These results suggested that the NAD-dependent modification of the 31-kDa protein was due to ADP-ribosylation of glycosylphosphatidylinositol-anchored RT6.1 at an arginine residue. When intact lymphocytes, in which RT6.1 had been once modified by [P]ADP-ribosylation, were further incubated in the absence of NAD, there was reduction of the radioactivity in the [P]ADP-ribosylated RT6.1. The reduced radioactivity was recovered from the incubation medium as [P]ADP-ribose. This reduction was effectively inhibited by the addition of ADP-ribose to the reaction mixture. Moreover, readdition of NAD caused the ADP-ribosylation of RT6.1 again. Thus, the ADP-ribosylation of RT6.1 appeared to proceed reversibly in intact rat lymphocytes.
登录
查看更多内容
外烟酰胺腺嘌呤二核苷酸 (NAD) 对细胞毒性 T 细胞的调节与细胞表面 GPI 锚定/精氨酸 ADP-核糖基转移酶相关。
DOI：
--
发表时间：
1994
期刊：
Journal of immunology (Baltimore, Md. : 1950)
影响因子：
--
作者：
Wang,J;Nemoto,E;Kots,AY;Kaslow,HR;Dennert,G
通讯作者：
Dennert,G
易患糖尿病的 BB/W 大鼠缺乏 RT-6 T 细胞亚群。
DOI：
--
发表时间：
1986
期刊：
Journal of immunology (Baltimore, Md. : 1950)
影响因子：
--
作者：
Greiner,DL;Handler,ES;Nakano,K;Mordes,JP;Rossini,AA
通讯作者：
Rossini,AA
骨骼肌微粒体膜精氨酸特异性 ADP-核糖基转移酶的纯化和部分表征。
DOI：
--
发表时间：
1990
期刊：
The Journal of biological chemistry
影响因子：
--
作者：
Peterson,JE;Larew,JS;Graves,DJ
通讯作者：
Graves,DJ
RT6 T 淋巴细胞在汞诱导的肾自身免疫中的作用：“易感”和“耐药”大鼠的实验操作。
DOI：
10.1080/15287399409531881
发表时间：
1994
期刊：
Journal of toxicology and environmental health
影响因子：
--
作者：
Kosuda,LL;Hosseinzadeh,H;Greiner,DL;Bigazzi,PE
通讯作者：
Bigazzi,PE