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. Author manuscript; available in PMC: 2012 Aug 25.
Published in final edited form as: Neuroscience. 2011 May 19;189:305–315. doi: 10.1016/j.neuroscience.2011.05.027

Figure 5. Glutamate induced ADAR2 cleavage is blocked by calpain inhibitor.

Figure 5

A. Cortical neurons expressing exogenous ADAR2 were either not treated or were treated with glutamate, or glutamate and plus the proteosome inhibitors such as MG132 or epoxomicin, or with glutamate and the caspase inhibitors zVAD or caspase inhibitor 3 or caspase 3 inhibitor, or with glutamate and calpain inhibitor (Figure 5A). Untreated neurons did not show ADAR2 cleavage (lane 1). Glutamate treatment resulted in ADAR2 cleavage (lane 2), and the proteosome/calpain inhibitor MG132 blocked ADAR2 cleavage (lane 4). However, another proteosome inhibitor, epoxomicin, did not block ADAR2 cleavage, and none of the caspase inhibitors, zVAD, caspase inhibitor III or caspase 3 inhibitor blocked the cleavage (lane 6, 7 and 8). Interestingly, calpain inhibitor I blocked ADAR2 cleavage (lane 3).

B. Cortical neurons expressing ADAR2 were treated with glutamate as described above using the two-calpain inhibitors. Calpain inhibitor I (lane 2) and calpain inhibitor X (lane 3) both blocked glutamate induced ADAR2 cleavage.