Danno S, Nishiyama H, Higashitsuji H, Yokoi H, Xue J H, Itoh K, Matsuda T, Fujita J
Department of Clinical Molecular Biology, Faculty of Medicine, Kyoto University, Sakyo-ku, Japan.
Biochem Biophys Res Commun. 1997 Jul 30;236(3):804-7. doi: 10.1006/bbrc.1997.7059.
Although the cold-shock responses of microorganisms have been extensively investigated, those of mammalian cells are just beginning to be understood. Recently, CIRP, a member of the glycine-rich RNA-binding protein (GRP) family, has been identified as the first cold-shock protein in mammalian cells. Here, we report that RBM3, another member of the GRP family, is induced in human cells in response to cold stress (32 degrees C). RBM3 transcripts were constitutively expressed in all cell lines examined including K562, HepG2, NC65, HeLa, and T24 cells. In all of them, the transcript levels of RBM3 were increased at 24 h after the 37 to 32 degrees C temperature down-shift. In NC65 cells, the kinetics of RBM3 induction was different from that of CIRP. Protein synthesis inhibitors cycloheximide and puromycin induced RBM3 transcripts, but cadmium chloride, H2O2, ethanol, and osmotic shock had no effect. Combined with the different tissue distribution of expression, these results suggest that RBM3 and CIRP play distinct roles in cold responses of human cells.
尽管微生物的冷休克反应已得到广泛研究,但哺乳动物细胞的冷休克反应才刚刚开始被了解。最近,富含甘氨酸的RNA结合蛋白(GRP)家族成员CIRP已被确定为哺乳动物细胞中的首个冷休克蛋白。在此,我们报告GRP家族的另一个成员RBM3在人类细胞中因冷应激(32摄氏度)而被诱导。RBM3转录本在包括K562、HepG2、NC65、HeLa和T24细胞在内的所有检测细胞系中组成性表达。在所有这些细胞系中,温度从37摄氏度降至32摄氏度后24小时,RBM3的转录水平均升高。在NC65细胞中,RBM3诱导的动力学与CIRP不同。蛋白质合成抑制剂放线菌酮和嘌呤霉素可诱导RBM3转录本,但氯化镉、过氧化氢、乙醇和渗透压休克则无影响。结合不同的组织表达分布,这些结果表明RBM3和CIRP在人类细胞的冷反应中发挥不同作用。