期刊
JOURNAL OF PROTEOME RESEARCH
卷 9, 期 4, 页码 1659-1669出版社
AMER CHEMICAL SOC
DOI: 10.1021/pr9006987
关键词
Spinal muscular atrophy; Survival motor neuron; Tandem affinity purification; Annexin; MRLC
资金
- Canadian Institutes of Health Research (CIHR)
- Muscular Dystrophy Association
- Families of SMA Canada (FSMAC)
- Ontario Graduate Scholarship
- University of Ottawa
Mutations in the survival motor neuron (SMN) gene cause spinal muscular atrophy (SMA), a neuromuscular disease associated with muscle weakness that progresses to paralysis, respiratory distress, and ultimately death. Both neurons and muscle are severely affected in this disease. Tandem affinity purification (TAP) has emerged as a useful tool for studying protein complexes in vitro. We have used this purification system to discover novel SMN interacting partners in C2C12 muscle and PC12 neuronal cells. To do so, we fused a TAP-tag, consisting of a HIS hexamer and FLAG epitope separated by the tobacco etch virus (TEV) protease cleavage site, to either the N- or C-terminal region of SMN. Interestingly, the profile of SMN interacting proteins varies depending on the cell type and stage. We have identified a number of novel SMN interacting proteins in both C2C12 and PC12 cells, and from among these we have validated Annexin II and myosin regulatory light chain (MRLC). The discovery of these proteins will lead to a better understanding of the mechanisms underlying the pathophysiology of SMA.
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