I6034
α-L-Iduronidase human
recombinant, expressed in mouse NSO cells
Synonym(s):
IDUA
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recombinant
expressed in mouse NSO cells
Quality Level
form
solution
specific activity
≥7,500 units/μg protein
mol wt
83 kDa
impurities
≤1.0 EU/μg Endotoxin
shipped in
wet ice
storage temp.
−20°C
Related Categories
General description
α-L-Iduronidase (IDUA) is mapped to human chromosome 4p16.3. The mature IDUA protein is glycosylated and comprises triosephosphate isomerase (TIM) barrel domain, β-sandwich, helix-loop-helix region and an immunoglobin-like domain.[1] α-L-Iduronidase is classified under glycoside hydrolase (GH) family 39.[2]
Application
α-L-Iduronidase may be used for leukocyte assay in the study of a-L-Iduronidase deficiency in new born.[3]
Biochem/physiol Actions
Catalyzes the hydrolysis of unsulfated α-L-iduronosidic linkages in dermatan sulfate
In lysosomal degradation process α-L-Iduronidase plays a crucial role. It hydrolyzes the non-reducing terminal α-L-iduronic acid residues in glycosaminoglycans (GAGs), including dermatan sulfate and heparan sulfate.[4]
Physical properties
Expressed as C-terminal histine-tagged protein (residues 1-653) with a caluclated molecular mass of 71 kDa migrating at ~83 kDa under SDS-PAGE reducing conditions.
Unit Definition
One unit will produce 1 picomole of 4-methylumbelliferone from 4-methylumbelliferyl-α-L-iduronide per minute at pH 3.5 at 25 °C.
Physical form
Supplied as a solution in 40 mM sodium acetate , 400 mM NaCl and 20% (v/v) glycerol, pH 5.0
Storage Class Code
10 - Combustible liquids
WGK
WGK 1
Flash Point(F)
Not applicable
Flash Point(C)
Not applicable
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Diagnosis of alpha-L-iduronidase deficiency in dried blood spots on filter paper: the possibility of newborn diagnosis.
N A Chamoles et al.
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Our objective was to assess how the diagnosis and treatment of mucopolysaccharidosis I (MPS I) have changed over time. We used data from 891 patients in the MPS I Registry, an international observational database, to analyze ages at symptom onset
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Mucopolysaccharidosis type I (MPS I) is traditionally divided into three phenotypes: the severe Hurler (MPS I-H) phenotype, the intermediate Hurler-Scheie (MPS I-H/S) phenotype and the attenuated Scheie (MPS I-S) phenotype. However, there are no clear criteria for delineating the different
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