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Analysis of SMN-neurite granules : core Cajal body components are absent from SMN-cytoplasmic complexes

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Todd, Adrian G., Morse, Robert, Shaw, Debra J., Stebbings, Howard and Young, Philip J. (2010) Analysis of SMN-neurite granules : core Cajal body components are absent from SMN-cytoplasmic complexes. Biochemical and Biophysical Research Communications, 397 (3). pp. 479-485. doi:10.1016/j.bbrc.2010.05.139 ISSN 0006-291X.

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Official URL: http://dx.doi.org/10.1016/j.bbrc.2010.05.139

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Abstract

Childhood spinal muscular atrophy (SMA) is caused by a reduction in survival motor neuron (SMN) protein. SMN is a ubiquitously expressed house keeping protein that is involved in RNA production and processing. However, although SMN is expressed in every cell type, only the lower motor neurons of the spinal cord are degraded in SMA. It remains unclear why this is the case. Recently, SMN has been linked to the axonal transport of β-actin mRNA from the cell body down to the growth cones. β-Actin is transported actively in neurite granules (NGs). However, it remains unclear which known SMN-binding partners are present in these SMN-NGs. To address this we have analysed SMN-NGs in a human neuronal cell line, SH-SY5Y, using antibodies against the majority of reported SMN-binding partners, including: Gemin2, Gemin3, Gemin4, Gemin5, Gemin6, Gemin7, Sm core proteins, fibrillarin, EWS, PFNII, Unrip and ZPR1. The obtained results highlight the metamorphic nature of the SMN complex, suggesting that not all the “core” SMN-binding proteins are transported in SMN-NGs.

Item Type: Journal Article
Divisions: Faculty of Science, Engineering and Medicine > Science > Life Sciences (2010- )
Journal or Publication Title: Biochemical and Biophysical Research Communications
Publisher: Elsevier
ISSN: 0006-291X
Official Date: 2 July 2010
Dates:
DateEvent
2 July 2010Published
Volume: 397
Number: 3
Page Range: pp. 479-485
DOI: 10.1016/j.bbrc.2010.05.139
Status: Peer Reviewed
Publication Status: Published
Access rights to Published version: Restricted or Subscription Access

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