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Pathologic alteration in the proteome of synaptosomes from the mouse model of spinal muscular atrophy

ABSTRACT: In this study, label-free quantitative proteomic analysis was performed using the Smn 2B/- mouse model to identify and investigate significant changes in protein abundance that may be related to the pathogenesis and neurodegeneration oberved in spinal muscular atrophy (SMA)

INSTRUMENT(S): Synapt MS

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Spinal Cord

DISEASE(S): Spinal Muscular Atrophy

SUBMITTER: Robert Gombar

LAB HEAD: Panayiotis O. Vacratsis

PROVIDER: PXD012850 | Pride | 2019-07-04

REPOSITORIES: Pride

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			Action	DRS
	Control_A1_001.msE.zip	Other
	Control_A1_001.raw.zip	Raw
	Control_A1_002.msE.zip	Other
	Control_A1_002.raw.zip	Raw
	Control_A1_003.msE.zip	Other

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Pathologic Alterations in the Proteome of Synaptosomes from a Mouse Model of Spinal Muscular Atrophy.

Eshraghi Mehdi M Gombar Robert R De Repentigny Yves Y Vacratsis Panayiotis O PO Kothary Rashmi R

Journal of proteome research 20190711 8

Spinal muscular atrophy (SMA) is a human genetic disorder characterized by muscle weakness, muscle atrophy, and death of motor neurons. SMA is caused by mutations or deletions in a gene called survival motor neuron 1 (SMN1). SMN1 is a housekeeping gene, but the most prominent pathologies in SMA are atrophy of myofibers and death of motor neurons. Further, degeneration of neuromuscular junctions, of synapses, and of axonal regions are features of SMA disease. Here, we have in ...[more]

PMID: 31262178

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