Arita Kyouhei, Hashimoto Hiroshi, Shimizu Toshiyuki, Nakashima Katsuhiko, Yamada Michiyuki, Sato Mamoru
Graduate School of Integrated Science, Yokohama City University, 1-7-29 Suehiro-cho, Tsurumi-ku, Yokohama 230-0045, Japan.
Nat Struct Mol Biol. 2004 Aug;11(8):777-83. doi: 10.1038/nsmb799. Epub 2004 Jul 11.
Peptidylarginine deiminase 4 (PAD4) is a Ca(2+)-dependent enzyme that catalyzes the conversion of protein arginine residues to citrulline. Its gene is a susceptibility locus for rheumatoid arthritis. Here we present the crystal structure of Ca(2+)-free wild-type PAD4, which shows that the polypeptide chain adopts an elongated fold in which the N-terminal domain forms two immunoglobulin-like subdomains, and the C-terminal domain forms an alpha/beta propeller structure. Five Ca(2+)-binding sites, none of which adopt an EF-hand motif, were identified in the structure of a Ca(2+)-bound inactive mutant with and without bound substrate. These structural data indicate that Ca(2+) binding induces conformational changes that generate the active site cleft. Our findings identify a novel mechanism for enzyme activation by Ca(2+) ions, and are important for understanding the mechanism of protein citrullination and for developing PAD-inhibiting drugs for the treatment of rheumatoid arthritis.
肽基精氨酸脱亚氨酶4(PAD4)是一种依赖钙离子的酶,可催化蛋白质精氨酸残基转化为瓜氨酸。其基因是类风湿性关节炎的一个易感位点。在此,我们展示了无钙离子的野生型PAD4的晶体结构,该结构表明多肽链呈现出一种拉长的折叠形式,其中N端结构域形成两个免疫球蛋白样亚结构域,C端结构域形成一个α/β螺旋桨结构。在结合和未结合底物的钙离子结合失活突变体结构中,鉴定出了五个钙离子结合位点,其中没有一个采用EF手基序。这些结构数据表明,钙离子结合会诱导构象变化,从而产生活性位点裂隙。我们的研究结果确定了钙离子激活酶的一种新机制,对于理解蛋白质瓜氨酸化的机制以及开发用于治疗类风湿性关节炎的PAD抑制药物具有重要意义。