Please use this identifier to cite or link to this item:
|Title:||Early induction of calpains in rotenone-mediated neuronal apoptosis||Authors:||Chen, M.J.
Cell cycle re-entry
|Issue Date:||2006||Citation:||Chen, M.J., Yap, Y.W., Choy, M.S., Koh, C.H.V., Seet, S.J., Duan, W., Whiteman, M., Cheung, N.S. (2006). Early induction of calpains in rotenone-mediated neuronal apoptosis. Neuroscience Letters 397 (1-2) : 69-73. ScholarBank@NUS Repository. https://doi.org/10.1016/j.neulet.2005.12.011||Abstract:||Rotenone is an inhibitor of mitochondrial complex I that produces a model of Parkinson's disease (PD), where neurons undergo apoptosis by caspase-dependent and/or caspase-independent pathways. Inhibition of calpains has recently been shown to attenuate neuronal apoptosis. This study aims to establish for the first time, the time-point of calpain activation with respect to the caspase activation and the possibility of cell cycle re-entry in rotenone-mediated cell death. Immunoblot results revealed calpain activation occurred at 5, 10 h prior to caspase-3 activation (at 15 h), suggesting calpain activation was an earlier cellular event compared to caspase activation in the rotenone-mediated apoptosis. In addition, an upregulation of phospho-p53 was observed at 21 h. However, no expression or upregulation of cell cycle regulatory proteins including cdc25a, cyclin-D1 and cyclin-D3 were observed, strongly suggesting that cell cycle re-entry did not occur. These findings provide new insights into the differential patterns of calpain and caspase activation that result from rotenone poisoning and which may be relevant to the therapeutic management of PD. © 2005 Elsevier Ireland Ltd. All rights reserved.||Source Title:||Neuroscience Letters||URI:||http://scholarbank.nus.edu.sg/handle/10635/28564||ISSN:||03043940||DOI:||10.1016/j.neulet.2005.12.011|
|Appears in Collections:||Staff Publications|
Show full item record
Files in This Item:
There are no files associated with this item.
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.