Literature DB >> 24480078

Structural and clinical implications of amino acid substitutions in α-L-iduronidase: insight into the basis of mucopolysaccharidosis type I.

Seiji Saito1, Kazuki Ohno2, Nobuo Maita3, Hitoshi Sakuraba4.   

Abstract

Allelic mutations, predominantly missense ones, of the α-l-iduronidase (IDUA) gene cause mucopolysaccharidosis type I (MPS I), which exhibits heterogeneous phenotypes. These phenotypes are basically classified into severe, intermediate, and attenuated types. We previously examined the structural changes in IDUA due to MPS I by homology modeling, but the reliability was limited because of the low sequence identity. In this study, we built new structural models of mutant IDUAs due to 57 amino acid substitutions that had been identified in 27 severe, 1 severe-intermediate, 13 intermediate, 1 attenuated-intermediate and 15 attenuated type MPS I patients based on the crystal structure of human IDUA, which was recently determined by us. The structural changes were examined by calculating the root-mean-square distances (RMSD) and the number of atoms influenced by the amino acid replacements. The results revealed that the structural changes of the enzyme protein tended to be correlated with the severity of the disease. Then we focused on the structural changes resulting from amino acid replacements in the immunoglobulin-like domain and adjacent region, of which the structure had been missing in the IDUA model previously built. Coloring of atoms influenced by an amino acid substitution was performed in each case and the results revealed that the structural changes occurred in a region far from the active site of IDUA, suggesting that they affected protein folding. Structural analysis is thus useful for elucidation of the basis of MPS I.
© 2013.

Entities:  

Keywords:  Amino acid substitution; Mucopolysaccharidosis type I; Structural model; α-l-Iduronidase

Mesh:

Substances:

Year:  2013        PMID: 24480078     DOI: 10.1016/j.ymgme.2013.10.005

Source DB:  PubMed          Journal:  Mol Genet Metab        ISSN: 1096-7192            Impact factor:   4.797


  5 in total

1.  Neurocognitive and neuropsychiatric phenotypes associated with the mutation L238Q of the α-L-iduronidase gene in Hurler-Scheie syndrome.

Authors:  Alia Ahmed; Chester B Whitley; Renee Cooksley; Kyle Rudser; Stephanie Cagle; Nadia Ali; Kathleen Delaney; Brianna Yund; Elsa Shapiro
Journal:  Mol Genet Metab       Date:  2013-12-12       Impact factor: 4.797

Review 2.  X-Ray Crystallography in Structure-Function Characterization of Therapeutic Enzymes.

Authors:  Anastassios C Papageorgiou
Journal:  Adv Exp Med Biol       Date:  2019       Impact factor: 2.622

3.  A longitudinal study of neurocognition and behavior in patients with Hurler-Scheie syndrome heterozygous for the L238Q mutation.

Authors:  Alia Ahmed; Li Ou; Kyle Rudser; Elsa Shapiro; Julie B Eisengart; Kelly King; Agnes Chen; Patricia Dickson; Chester B Whitley
Journal:  Mol Genet Metab Rep       Date:  2019-06-27

4.  Identification of a novel compound heterozygous IDUA mutation underlies Mucopolysaccharidoses type I in a Chinese pedigree.

Authors:  Yong-An Zhou; Ping Li; Yanping Zhang; Qiuhong Xiong; Chao Li; Zhonghua Zhao; Yuxian Wang; Han Xiao
Journal:  Mol Genet Genomic Med       Date:  2019-11-23       Impact factor: 2.183

5.  A deletion of IDUA exon 10 in a family of Golden Retriever dogs with an attenuated form of mucopolysaccharidosis type I.

Authors:  Kiterie M E Faller; Alison E Ridyard; Rodrigo Gutierrez-Quintana; Angie Rupp; Celia Kun-Rodrigues; Tatiana Orme; Karen L Tylee; Heather J Church; Rita Guerreiro; Jose Bras
Journal:  J Vet Intern Med       Date:  2020-08-12       Impact factor: 3.333

  5 in total

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