Processing of cdk5 activator p35 to its truncated form (p25) by calpain in acutely injured neuronal cells.

@article{Nath2000ProcessingOC,
  title={Processing of cdk5 activator p35 to its truncated form (p25) by calpain in acutely injured neuronal cells.},
  author={Rathna Nath and M O Davis and Albert W. Probert and Nancy C. Kupina and Xiao Dan Ren and Gerald P. Schielke and K. K. W. Wang},
  journal={Biochemical and biophysical research communications},
  year={2000},
  volume={274 1},
  pages={
          16-21
        }
}
  • R. Nath, M. Davis, +4 authors K. Wang
  • Published 21 July 2000
  • Biology, Chemistry
  • Biochemical and biophysical research communications
Recently, it was shown that conversion of cdk5 activator protein p35 to a C-terminal fragment p25 promotes a deregulation of cdk5 activity, which may contribute to neurodegeneration in Alzheimer's disease. In this study, we present evidence that calpain is a protease involved in the conversion of p35 to p25. To activate calpain, rat cerebellar granule neurons were treated with maitotoxin (MTX). A C-terminus-directed anti-p35 antibody detected that p35 conversion to p25 paralleled the formation… 
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TLDR
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References

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