Cardiac involvement in Anderson-Fabry disease
Anderson-Fabry disease results from hereditary deficiency of the lysosomal enzyme α-galactosidase A. This disease is marked by progressive intracellular accumulation of globotriaosylceramide (Gb3) and digalactosylceramide, the major glycosphingolipid substrates of α-galactosidase A. Many cell
Gespeichert in:
| Hauptverfasser: | , , , |
|---|---|
| Dokumenttyp: | Article (Journal) |
| Sprache: | Englisch |
| Veröffentlicht: |
June 2002
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| In: |
Journal of the American Society of Nephrology
Year: 2002, Jahrgang: 13, Pages: S147-S149 |
| ISSN: | 1533-3450 |
| DOI: | 10.1097/01.ASN.0000015238.98011.AF |
| Online-Zugang: | Verlag, Volltext: https://doi.org/10.1097/01.ASN.0000015238.98011.AF Verlag, Volltext: https://jasn.asnjournals.org/content/13/suppl_2/S147 
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| Verfasserangaben: | Christoph Kampmann, Frank Baehner, Markus Ries, and Michael Beck |
MARC
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| 520 | |a Anderson-Fabry disease results from hereditary deficiency of the lysosomal enzyme α-galactosidase A. This disease is marked by progressive intracellular accumulation of globotriaosylceramide (Gb3) and digalactosylceramide, the major glycosphingolipid substrates of α-galactosidase A. Many cell | ||
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