Abstract
Calpain-mediated cleavage of neuronal targets has long been associated with excitotoxicity and synaptic plasticity. In this issue of Neuron, two papers by Xu et al. and Abe and Takeichi explore the respective roles of mGluR1alpha cleavage in excitotoxicity and beta-catenin cleavage in transcriptional control. Together, these papers show the functional importance of fragments of calpain-mediated cleavage.
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