Pages that link to "Q28593569"
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The following pages link to Late onset Tay-Sachs disease in mice with targeted disruption of the Hexa gene: behavioral changes and pathology of the central nervous system (Q28593569):
Displaying 15 items.
- Hexosaminidase A (Q21984075) (← links)
- Long-term correction of Sandhoff disease following intravenous delivery of rAAV9 to mouse neonates (Q27318381) (← links)
- Mice Doubly-Deficient in Lysosomal Hexosaminidase A and Neuraminidase 4 Show Epileptic Crises and Rapid Neuronal Loss (Q27346357) (← links)
- Gene transfer corrects acute GM2 gangliosidosis--potential therapeutic contribution of perivascular enzyme flow (Q30523995) (← links)
- Dysregulation of the ALS-associated gene TDP-43 leads to neuronal death and degeneration in mice (Q34519947) (← links)
- Mice, double deficient in lysosomal serine carboxypeptidases Scpep1 and Cathepsin A develop the hyperproliferative vesicular corneal dystrophy and hypertrophic skin thickenings. (Q36289890) (← links)
- Sphingolipids and membrane biology as determined from genetic models (Q36459028) (← links)
- Clinical features and molecular genetics of autosomal recessive cerebellar ataxias (Q36736797) (← links)
- Behavioural and pharmacological examinations in a transgenic mouse model of early-onset torsion dystonia (Q42813363) (← links)
- Deletion of tumor necrosis factor-α ameliorates neurodegeneration in Sandhoff disease mice. (Q45928684) (← links)
- Spontaneous appearance of Tay-Sachs disease in an animal model (Q46436089) (← links)
- Isolation, sequence identification and tissue expression profiles of 3 novel porcine genes: ASPA, NAGA, and HEXA. (Q46453110) (← links)
- Mice deficient in Neu4 sialidase exhibit abnormal ganglioside catabolism and lysosomal storage (Q46757649) (← links)
- GM2 gangliosidosis associated with a HEXA missense mutation in Japanese Chin dogs: a potential model for Tay Sachs disease (Q48241353) (← links)
- Conditional LoxP-flanked glucosylceramide synthase allele controlling glycosphingolipid synthesis (Q48698146) (← links)