| Literature DB >> 18421424 |
Tatiana I Samoylova1, Douglas R Martin, Nancy E Morrison, Misako Hwang, Anna M Cochran, Alexandre M Samoylov, Henry J Baker, Nancy R Cox.
Abstract
Lysosomal beta-galactosidase is required for the degradation of GM1 ganglioside and other glycolipids and glycoproteins with a terminal galactose moiety. Deficiency of this enzyme leads to the lysosomal storage disorder, GM1 gangliosidosis, marked by severe neurodegeneration resulting in premature death. As a step towards preclinical studies for enzyme replacement therapy in an animal model of GM1 gangliosidosis, a feline beta-galactosidase cDNA was cloned into a mammalian expression vector and subsequently expressed in Chinese hamster ovary (CHO-K1) cells. The enzyme secreted into culture medium exhibited specific activity on two synthetic substrates as well as on the native beta-galactosidase substrate, GM1 ganglioside. The enzyme was purified from transfected CHO-K1 cell culture medium by chromatography on PATG-agarose. The affinity-purified enzyme preparation consisted mainly of the protein with approximate molecular weight of 94 kDa and displayed immunoreactivity with antibodies raised against a 16-mer synthetic peptide corresponding to C-terminal amino acid sequence deduced from the feline beta-galactosidase cDNA.Entities:
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Year: 2008 PMID: 18421424 DOI: 10.1007/s11011-008-9086-5
Source DB: PubMed Journal: Metab Brain Dis ISSN: 0885-7490 Impact factor: 3.584