From the Graduate School of Pharmaceutical Sciences, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-0033, Japan.
J Biol Chem. 2012 Jan 13;287(3):1801-12. doi: 10.1074/jbc.M111.293795. Epub 2011 Nov 28.
G(M1) gangliosidosis and Morquio B are autosomal recessive lysosomal storage diseases associated with a neurodegenerative disorder or dwarfism and skeletal abnormalities, respectively. These diseases are caused by deficiencies in the lysosomal enzyme β-d-galactosidase (β-Gal), which lead to accumulations of the β-Gal substrates, G(M1) ganglioside, and keratan sulfate. β-Gal is an exoglycosidase that catalyzes the hydrolysis of terminal β-linked galactose residues. This study shows the crystal structures of human β-Gal in complex with its catalytic product galactose or with its inhibitor 1-deoxygalactonojirimycin. Human β-Gal is composed of a catalytic TIM barrel domain followed by β-domain 1 and β-domain 2. To gain structural insight into the molecular defects of β-Gal in the above diseases, the disease-causing mutations were mapped onto the three-dimensional structure. Finally, the possible causes of the diseases are discussed.
G(M1)神经节苷脂贮积症和 Morquio B 型是两种常染色体隐性溶酶体贮积病,分别与神经退行性疾病或矮小症和骨骼异常有关。这些疾病是由溶酶体酶β-D-半乳糖苷酶(β-Gal)的缺乏引起的,导致β-Gal 底物 G(M1)神经节苷脂和硫酸角质素的积累。β-Gal 是一种外糖苷酶,可催化末端β-linked 半乳糖残基的水解。本研究展示了人β-Gal 与其催化产物半乳糖或抑制剂 1-脱氧半乳糖基氮杂环庚烷的复合物的晶体结构。人β-Gal 由一个催化 TIM 桶结构域和β-结构域 1 和β-结构域 2 组成。为了深入了解上述疾病中β-Gal 的分子缺陷,将致病突变映射到三维结构上。最后,讨论了疾病的可能原因。