Laboratory of Cell Signaling, Graduate School of Pharmaceutical Sciences, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-0033, Japan.
Department of Data Science, The Institute of Statistical Mathematics, 10-3 Midori-cho, Tachikawa, Tokyo 190-8562, Japan.
Database (Oxford). 2024 Aug 8;2024:0. doi: 10.1093/database/baae064.
A structural alteration in copper/zinc superoxide dismutase (SOD1) is one of the common features caused by amyotrophic lateral sclerosis (ALS)-linked mutations. Although a large number of SOD1 variants have been reported in ALS patients, the detailed structural properties of each variant are not well summarized. We present SoDCoD, a database of superoxide dismutase conformational diversity, collecting our comprehensive biochemical analyses of the structural changes in SOD1 caused by ALS-linked gene mutations and other perturbations. SoDCoD version 1.0 contains information about the properties of 188 types of SOD1 mutants, including structural changes and their binding to Derlin-1, as well as a set of genes contributing to the proteostasis of mutant-like wild-type SOD1. This database provides valuable insights into the diagnosis and treatment of ALS, particularly by targeting conformational alterations in SOD1. Database URL: https://fujisawagroup.github.io/SoDCoDweb/.
铜/锌超氧化物歧化酶 (SOD1) 的结构改变是由肌萎缩侧索硬化症 (ALS) 相关突变引起的常见特征之一。尽管在 ALS 患者中已经报道了大量的 SOD1 变体，但每个变体的详细结构特性尚未得到很好的总结。我们提出了 SoDCoD，这是一个超氧化物歧化酶构象多样性数据库，收集了我们对 ALS 相关基因突变和其他扰动引起的 SOD1 结构变化的全面生化分析。SoDCoD 版本 1.0 包含了 188 种 SOD1 突变体的特性信息，包括结构变化及其与 Derlin-1 的结合，以及一组有助于突变型类似野生型 SOD1 蛋白稳态的基因。该数据库为 ALS 的诊断和治疗提供了有价值的见解，特别是通过针对 SOD1 的构象改变。数据库网址：https://fujisawagroup.github.io/SoDCoDweb/。
