|1.||Sena-Esteves, M: 3 articles (02/2009 - 03/2000)|
|2.||Beck, M: 2 articles (09/2010 - 08/2001)|
|3.||Paschke, E: 2 articles (09/2010 - 08/2001)|
|4.||Michelakakis, H: 2 articles (09/2010 - 08/2001)|
|5.||Broekman, M L D: 2 articles (02/2009 - 01/2007)|
|6.||Yamasaki, Masahiro: 2 articles (02/2007 - 02/2003)|
|7.||Yonemura, Madoka: 2 articles (02/2007 - 02/2003)|
|8.||Satoh, Hiroyuki: 2 articles (02/2007 - 02/2003)|
|9.||Asano, Tomoya: 2 articles (02/2007 - 02/2003)|
|10.||Yamato, Osamu: 2 articles (02/2007 - 02/2003)|
|2.||GM1 Gangliosidosis (Gangliosidosis GM1)
02/01/2003 - "The present study was conducted to determine the clinical and clinico-pathologic characteristics of Shiba dogs with GM1 gangliosidosis, which is due to an autosomal recessively inherited deficiency of lysosomal acid beta-galactosidase activity. "
11/01/2004 - "Deficiency of enzyme acid beta-galactosidase causes GM1 gangliosidosis. "
02/01/2003 - "Clinical and clinico-pathologic characteristics of Shiba dogs with a deficiency of lysosomal acid beta-galactosidase: a canine model of human GM1 gangliosidosis."
07/01/2000 - "In contrast, twitcher mice with a single functional acid beta-galactosidase gene have the most severe disease with the shortest lifespan, despite the fact that G(M1) gangliosidosis carrier mice with an otherwise normal genetic background are phenotypically normal. "
03/20/2000 - "Correction of acid beta-galactosidase deficiency in GM1 gangliosidosis human fibroblasts by retrovirus vector-mediated gene transfer: higher efficiency of release and cross-correction by the murine enzyme."
|3.||Wounds and Injuries (Trauma)
|4.||Mucopolysaccharidosis IV (Morquio Syndrome)
01/01/2003 - "G(M1)-gangliosidosis and Morquio B disease are distinct in clinical and biochemical features, but both disorders are caused by genetic defects of the same enzyme, acid beta-galactosidase (beta-Gal). "
08/01/2001 - "Mutation analyses in 17 patients with deficiency in acid beta-galactosidase: three novel point mutations and high correlation of mutation W273L with Morquio disease type B."
12/01/1995 - "beta-galactosidosis is a lysosomal storage disorder caused by a deficiency of acid beta-galactosidase, including to autosomal recessive diseases; GM1-gangliosidosis (neurovisceral form) and Morquio B disease (skeletal form). "
01/01/1994 - "The lysosomal storage disorders GM1-gangliosidosis and Morquio B syndrome are caused by a complete or partial deficiency of acid beta-galactosidase. "
11/30/1982 - "Morquio disease, type B: activation of GM1-beta-galactosidase by GM1-activator protein."
|5.||Lysosomal Storage Diseases (Lysosomal Storage Disease)
01/01/2007 - "GM1-gangliosidosis is a glycosphingolipid (GSL) lysosomal storage disease caused by autosomal recessive deficiency of lysosomal acid beta-galactosidase (betagal), and characterized by accumulation of GM1-ganglioside and GA1 in the brain. "
01/01/1999 - "GM1-gangliosidosis is a lysosomal storage disease caused by a deficiency of acid beta-galactosidase. "
01/01/2010 - "GM1 gangliosidosis (GM1) is an autosomal recessive lysosomal storage disease caused by deficiency of acid beta-galactosidase (GLB1; EC126.96.36.199). "
02/16/2007 - "GM1 gangliosidosis, a lysosomal storage disease that affects the brain and multiple systemic organs, is due to an autosomal recessively inherited deficiency of acid beta-galactosidase activity. "
05/01/2004 - "GM1 gangliosidosis is a glycosphingolipid (GSL) lysosomal storage disease caused by a genetic deficiency of acid beta-galactosidase (beta-gal), the enzyme that catabolyzes GM1 within lysosomes. "
|1.||Fluorescent Dyes (Fluorescent Probes)
|7.||Citric Acid (Citrate)
|8.||Complementary DNA (cDNA)
|9.||Taurocholic Acid (Sodium Taurocholate)