Deletion of tumor necrosis factor-α ameliorates neurodegeneration in Sandhoff disease mice

Author:

Abo-ouf Hatem1,Hooper Alexander WM1,White Elizabeth J1,Janse van Rensburg Helena J1,Trigatti Bernardo L2,Igdoura Suleiman A13

Affiliation:

1. Department of Biology,

2. Department of Biochemistry and Biomedical Sciences and

3. Department of Pathology and Molecular Medicine, McMaster University, Hamilton, Ontario, Canada

Publisher

Oxford University Press (OUP)

Subject

Genetics(clinical),Genetics,Molecular Biology,General Medicine

Reference55 articles.

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3. The human GM2 activator protein. A substrate specific cofactor of beta-hexosaminidase a;Meier;J. Biol. Chem.,1991

4. Ganglioside GM2 N-acetyl-beta-D-galactosaminidase activity in cultured fibroblasts of late-infantile and adult GM2 gangliosidosis patients and of healthy probands with low hexosaminidase level;Conzelmann;Am. J. Hum. Genet.,1983

5. Mouse models of Tay-Sachs and Sandhoff diseases differ in neurologic phenotype and ganglioside metabolism;Sango;Nat. Genet.,1995

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