The homozygous M712T mutation of UDP‐N‐acetylglucosamine 2‐epimerase/N‐acetylmannosamine kinase results in reduced enzyme activities but not in altered overall cellular sialylation in hereditary inclusion body myopathy
暂无分享,去创建一个
K. Yarema | W. Reutter | S. Mitrani‐Rosenbaum | T. Potikha | I. Eisenberg | M. Sadeh | L. Mantey | S. Hinderlich | R. Horstkorte | Z. Argov | I. Salama | Kevin J. Yarema | Lars R. Mantey | S. Mitrani-Rosenbaum | Lars R. Mantey
[1] I. Nonaka,et al. Reduction of UDP-N-acetylglucosamine 2-Epimerase/N-Acetylmannosamine Kinase Activity and Sialylation in Distal Myopathy with Rimmed Vacuoles* , 2004, Journal of Biological Chemistry.
[2] J. Mendell,et al. Mutations spectrum of GNE in hereditary inclusion body myopathy sparing the quadriceps , 2003, Human mutation.
[3] K. Knobeloch,et al. Sialylation is essential for early development in mice , 2002, Proceedings of the National Academy of Sciences of the United States of America.
[4] Hans-Joachim Gabius,et al. Glycosciences: Status and Perspectives , 2002 .
[5] Tsviya Olender,et al. The UDP-N-acetylglucosamine 2-epimerase/N-acetylmannosamine kinase gene is mutated in recessive hereditary inclusion body myopathy , 2001, Nature Genetics.
[6] M. Pawlita,et al. Evidence for efficient uptake and incorporation of sialic acid by eukaryotic cells. , 2001, European journal of biochemistry.
[7] M. Pawlita,et al. Biosynthesis of N-Acetylneuraminic Acid in Cells Lacking UDP-N-Acetylglucosamine 2-Epimerase/ N-Acetylmannosamine Kinase , 2001, Biological chemistry.
[8] W. Reutter,et al. Protein kinase C phosphorylates and regulates UDP‐N‐acetylglucosamine‐2‐epimerase/N‐acetylmannosamine kinase , 2000, FEBS letters.
[9] W. Reutter,et al. Selective Loss of either the Epimerase or Kinase Activity of UDP-N-acetylglucosamine 2-Epimerase/N-Acetylmannosamine Kinase due to Site-directed Mutagenesis Based on Sequence Alignments* , 1999, The Journal of Biological Chemistry.
[10] M. Pawlita,et al. UDP-GlcNAc 2-epimerase: a regulator of cell surface sialylation. , 1999, Science.
[11] S. Mitrani‐Rosenbaum,et al. Genetics of inclusion body myopathies. , 1998, Current opinion in rheumatology.
[12] W. Reutter,et al. A Bifunctional Enzyme Catalyzes the First Two Steps in N-Acetylneuraminic Acid Biosynthesis of Rat Liver , 1997, The Journal of Biological Chemistry.
[13] H. Gabius,et al. Sialic acids structure-analysis-metabolism-occurrence-recognition. , 1996, Biological chemistry Hoppe-Seyler.
[14] D. J. Wells,et al. Purification and characterization of a sialic acid-specific lectin from Tritrichomonas mobilensis. , 1994, The Biochemical journal.
[15] R. Hynes,et al. Contact and adhesive specificities in the associations, migrations, and targeting of cells and axons , 1992, Cell.
[16] Z. Argov,et al. “Rimmed vacuole myopathy” sparing the quadriceps A unique disorder in iranian jews , 1984, Journal of the Neurological Sciences.
[17] S. Roseman,et al. The sialic acids. XI. A periodate-resorcinol method for the quantitative estimation of free sialic acids and their glycosides. , 1971, The Journal of biological chemistry.
[18] J. Strominger,et al. A modified colorimetric method for the estimation of N-acetylamino sugars. , 1955, The Journal of biological chemistry.
[19] G. Edelman,et al. Cell adhesion molecules: implications for a molecular histology. , 1991, Annual review of biochemistry.