N-butyldeoxygalactonojirimycin reduces postnatal cerebellar ganglioside content in a mouse model of GM1 gangliosidosis

N-butyldeoxygalactonojirimycin reduces postnatal cerebellar ganglioside content in a mouse model of GM1 gangliosidosis

Bibliográfalaš dieđut
Váldodahkkit:	Kasperzyk, J, d'Azzo, A, Platt, F, Seyfried, T
Materiálatiipa:	Conference item
Almmustuhtton:	2004

Geahča maid

N-butyldeoxygalactonojirimycin reduces neonatal brain ganglioside content in a mouse model of GM1 gangliosidosis.
Dahkki: Kasperzyk, J, et al.
Almmustuhtton: (2004)

"Substrate reduction reduces gangliosides in postnatal cerebrum-brainstem and cerebellum in GM1 gangliosidosis mice" (vol 46, pg 744, 2004)
Dahkki: Kasperzyk, J, et al.
Almmustuhtton: (2005)

N-butyldeoxygalactonojirimycin reduces brain ganglioside and GM2 content in neonatal Sandhoff disease mice.
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Almmustuhtton: (2008)

N-butyldeoxygalactonojirimycin reduces brain ganglioside and GM2 content in neonatal sandhoff diseased mice
Dahkki: Baek, R, et al.
Almmustuhtton: (2004)

Erratum: Substrate reduction reduces gangliosides in postnatal cerebrum-brainstem and cerebellum in GM1 gangliosidosis mice (Journal of Lipid Research (April 2004) 46 (744-751))
Dahkki: Kasperzyk, J, et al.
Almmustuhtton: (2005)

Substrate deprivation therapy reduces brain ganglioside content and GM1 in neonatal storage disease mice
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Almmustuhtton: (2002)

Substrate reduction therapy reduces brain ganglioside GM2 in neonatal Sandhoff disease mice
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Central nervous system inflammation is a hallmark of pathogenesis in mouse models of GM1 and GM2 gangliosidosis.
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Beneficial effects of substrate reduction therapy in a mouse model of GM1 gangliosidosis.
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Therapeutic assessment of substrate deprivation using NB-DGJ in GM1 storage disease mice
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N -butyldeoxynojirimycin reduces growth and ganglioside content of experimental mouse brain tumours.
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Combined deficiencies of endosomal ganglioside neuraminidases 3 and 4 in mice cause lysosomal GM3 gangliosidosis
Dahkki: Pshezhetsky, A, et al.
Almmustuhtton: (2017)

Combined deficiencies of endosomal ganglioside neuraminidases 3 and 4 in mice cause lysosomal GM3 gangliosidosis
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Altered expression of ganglioside metabolizing enzymes results in GM3 ganglioside accumulation in cerebellar cells of a mouse model of juvenile neuronal ceroid lipofuscinosis
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Effects of substrate deprivation therapy on brain lipids in neonatal GML storage disease mice
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Improved outcome of N-butyldeoxygalactonojirimycin-mediated substrate reduction therapy in a mouse model of Sandhoff disease.
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GM1 Gangliosidosis Type 1 and Mongolian Spots
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GM1 ganglioside-independent intoxication by Cholera toxin
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N-butyldeoxygalactonojirimycin: a more selective inhibitor of glycosphingolipid biosynthesis than N-butyldeoxynojirimycin, in vitro and in vivo.
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Persistent elevations of alkaline phosphatase as an early indicator of GM1 gangliosidosis
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Extensive telangiectasias and mongolian spots: A clue towards GM1-gangliosidosis
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Elevation of ganglioside degradation pathway drives GM2 and GM3 within amyloid plaques in a transgenic mouse model of Alzheimer's disease
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Pathological findings of central nervous system, two GM1 gangliosidosis autopsy cases
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Clinical and imaging predictors of late‐onset GM2 gangliosidosis: A scoping review
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NGcGM3 Ganglioside: A Privileged Target for Cancer Vaccines
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Disease‐modifying effects of ganglioside GM1 in Huntington's disease models
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GM2 Gangliosidosis (Tay-Sachs Disease), type I, Infantile Form: Clinical Case
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Re: “Molecular analysis of 9 unrelated families presenting with juvenile and chronic GM1 gangliosidosis”
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Mutations in B4GALNT1 (GM2 synthase) underlie a new disorder of ganglioside biosynthesis
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GM1 Ganglioside Promotes Osteogenic Differentiation of Human Tendon Stem Cells
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Infantile Gangliosidosis
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Quantitative reliability assessment of brain MRI volumetric measurements in type II GM1 gangliosidosis patients
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Enhanced Susceptibility to Chemoconvulsant-Induced Seizures in Ganglioside GM3 Synthase Knockout Mice
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