Bayer P, Arndt A, Metzger S, Mahajan R, Melchior F, Jaenicke R, Becker J
Abteilung Physikalische Biochemie, Max-Planck-Institut für molekulare Physiologie, Dortmund, Germany.
J Mol Biol. 1998 Jul 10;280(2):275-86. doi: 10.1006/jmbi.1998.1839.
The recently discovered small ubiquitin-related modifier SUMO-1 belongs to the growing family of ubiquitin-related proteins involved in postranslational protein modification. Unlike ubiquitin, SUMO-1 does not appear to target proteins for degradation but seems to be involved in the modulation of protein-protein interactions. Independent studies demonstrate an essential function of SUMO-1 in the regulation of nucleo-cytoplasmic transport, and suggest a role in cell-cycle regulation and apoptosis. Here, we present the first three-dimensional structure of SUMO-1 solved by NMR. Although having only 18% amino acid sequence identity with ubiquitin, the overall structure closely resembles that of ubiquitin, featuring the betabetaalphabetabetaalphabeta fold of the ubiquitin protein family. In addition, the position of the two C-terminal Gly residues required for isopeptide bond formation is conserved between ubiquitin and SUMO-1. The most prominent feature of SUMO-1 is a long and highly flexible N terminus, which protrudes from the core of the protein and which is absent in ubiquitin. Furthermore, ubiquitin Lys48, required to generate ubiquitin polymers, is substituted in SUMO-1 by Gln69 at the same position, which provides an explanation of why SUMO-1 has not been observed to form polymers. Moreover, the hydrophobic core of SUMO-1 and ubiquitin is maintained by conserved hydrophobic residues, whereas the overall charge topology of SUMO-1 and ubiquitin differs significantly, suggesting specific modifying enzymes and target proteins for both proteins.
最近发现的小泛素相关修饰物SUMO-1属于参与蛋白质翻译后修饰的泛素相关蛋白家族,且该家族仍在不断扩大。与泛素不同,SUMO-1似乎并不将蛋白质作为降解靶点,而是参与蛋白质-蛋白质相互作用的调节。独立研究表明SUMO-1在核质运输调节中具有重要功能,并提示其在细胞周期调节和细胞凋亡中发挥作用。在此,我们展示了通过核磁共振解析得到的SUMO-1的首个三维结构。尽管SUMO-1与泛素只有18%的氨基酸序列同一性,但其整体结构与泛素非常相似,具有泛素蛋白家族的ββαββαβ折叠结构。此外,泛素和SUMO-1之间形成异肽键所需的两个C末端甘氨酸残基的位置是保守的。SUMO-1最显著的特征是一个长且高度灵活的N末端,它从蛋白质核心突出,而泛素中不存在该结构。此外,泛素生成泛素聚合物所需的赖氨酸48在SUMO-1中被相同位置的谷氨酰胺69取代,这解释了为何未观察到SUMO-1形成聚合物。而且,SUMO-1和泛素的疏水核心由保守的疏水残基维持,而SUMO-1和泛素的整体电荷拓扑结构有显著差异,这表明这两种蛋白质具有特定的修饰酶和靶蛋白。