Characterization of the human sialidase Neu4 gene promoter

* Correspondence: volkanseyrantepe@iyte.edu.tr

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Neu4, a novel human lysosomal lumen sialidase, confers normal phenotype to sialidosis and galactosialidosis cells.

Mice deficient in Neu4 sialidase exhibit abnormal ganglioside catabolism and lysosomal storage.

Molecular cloning and characterization of NEU4, the fourth member of the human sialidase gene family.

Human sialidase NEU4 long and short are extrinsic proteins bound to outer mitochondrial membrane and the endoplasmic reticulum, respectively.

Mice Doubly-Deficient in Lysosomal Hexosaminidase A and Neuraminidase 4 Show Epileptic Crises and Rapid Neuronal Loss

Aberrant expression of sialidase and cancer progression

Dramatically different phenotypes in mouse models of human Tay-Sachs and Sandhoff diseases.

Disruption of murine Hexa gene leads to enzymatic deficiency and to neuronal lysosomal storage, similar to that observed in Tay-Sachs disease

Mouse models of Tay–Sachs and Sandhoff diseases differ in neurologic phenotype and ganglioside metabolism

Characterization of the human sialidase Neu4 gene promoter

Neu4, a novel human lysosomal lumen sialidase, confers normal phenotype to sialidosis and galactosialidosis cells.

Biochemistry and function of sialidases

Mice deficient in Neu4 sialidase exhibit abnormal ganglioside catabolism and lysosomal storage.

Molecular cloning and characterization of NEU4, the fourth member of the human sialidase gene family.

Human sialidase NEU4 long and short are extrinsic proteins bound to outer mitochondrial membrane and the endoplasmic reticulum, respectively.

Mice Doubly-Deficient in Lysosomal Hexosaminidase A and Neuraminidase 4 Show Epileptic Crises and Rapid Neuronal Loss

Aberrant expression of sialidase and cancer progression

Dramatically different phenotypes in mouse models of human Tay-Sachs and Sandhoff diseases.

Disruption of murine Hexa gene leads to enzymatic deficiency and to neuronal lysosomal storage, similar to that observed in Tay-Sachs disease

Mouse models of Tay–Sachs and Sandhoff diseases differ in neurologic phenotype and ganglioside metabolism

Characterization of the human sialidase Neu4 gene promoter

Neu4, a novel human lysosomal lumen sialidase, confers normal phenotype to sialidosis and galactosialidosis cells.

Biochemistry and function of sialidases

Mice deficient in Neu4 sialidase exhibit abnormal ganglioside catabolism and lysosomal storage.

Molecular cloning and characterization of NEU4, the fourth member of the human sialidase gene family.

Human sialidase NEU4 long and short are extrinsic proteins bound to outer mitochondrial membrane and the endoplasmic reticulum, respectively.

Mice Doubly-Deficient in Lysosomal Hexosaminidase A and Neuraminidase 4 Show Epileptic Crises and Rapid Neuronal Loss

Aberrant expression of sialidase and cancer progression

Dramatically different phenotypes in mouse models of human Tay-Sachs and Sandhoff diseases.

Disruption of murine Hexa gene leads to enzymatic deficiency and to neuronal lysosomal storage, similar to that observed in Tay-Sachs disease

Mouse models of Tay–Sachs and Sandhoff diseases differ in neurologic phenotype and ganglioside metabolism