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Spinal muscular atrophy (SMA) is caused by a drastic reduction in the ubiquitously expressed SMN protein, which is critical for the correct assembly of the snRNP complexes required for RNA splicing. However, it is unclear why loss of SMN and altered snRNP assembly only seem to affect motor neurons. Reporting in this issue, Zhang et al. (2008) challenge prior assumptions about the housekeeping function of SMN and demonstrate that loss of SMN leads to highly tissue-specific effects on splicing.

Original publication

DOI

10.1016/j.cell.2008.05.002

Type

Journal article

Journal

Cell

Publication Date

16/05/2008

Volume

133

Pages

572 - 574

Keywords

Animals, Cyclic AMP Response Element-Binding Protein, Humans, Mice, Motor Neurons, Muscular Atrophy, Spinal, Nerve Tissue Proteins, RNA Splicing, RNA-Binding Proteins, Ribonucleoproteins, Small Nuclear, SMN Complex Proteins