Giancotti V, Bandiera A, Sindici C, Perissin L, Crane-Robinson C
Dipartimento di Biochimica, Biofisica e Chimica delle Macromolecole, Università di Trieste, Italy.
Biochem J. 1996 Aug 1;317 ( Pt 3)(Pt 3):865-70. doi: 10.1042/bj3170865.
Micrococcal nuclease digestion of nuclei from mouse Lewis lung carcinoma cells releases a protein mixture into the supernatant that lacks histone H1 and contains a full complement of high-mobility-group I (HMGI) proteins (i.e. I, Y and I-C). This implies that all three HMGI proteins are localized at the nuclease-sensitive regions of active chromatin. It is also shown that if Ca2+ ions are present in the nuclear incubation buffer (with or without exogenous nuclease), all three HMGI proteins become ADP-ribosylated. We propose that this modification of HMGI family proteins is part of the general poly(ADP-ribosyl)ation that accompanies DNA damage in apoptosis and other processes.
用微球菌核酸酶消化小鼠Lewis肺癌细胞核,会将一种缺乏组蛋白H1且含有完整高迁移率族I(HMGI)蛋白(即I、Y和I-C)的蛋白质混合物释放到上清液中。这意味着所有三种HMGI蛋白都定位于活性染色质的核酸酶敏感区域。研究还表明,如果在细胞核孵育缓冲液中存在Ca2+离子(无论有无外源性核酸酶),所有三种HMGI蛋白都会发生ADP-核糖基化。我们认为,HMGI家族蛋白的这种修饰是凋亡和其他过程中伴随DNA损伤的一般多(ADP-核糖基)化的一部分。