Note to users. If you're seeing this message, it means that your browser cannot find this page's style/presentation instructions -- or possibly that you are using a browser that does not support current Web standards. Find out more about why this message is appearing, and what you can do to make your experience of our site the best it can be.


Sci. Signal., 8 April 2008
Vol. 1, Issue 14, p. re1
[DOI: 10.1126/stke.114re1]

REVIEWS

Calpain in the CNS: From Synaptic Function to Neurotoxicity

Jing Liu1*, Ming Cheng Liu2,3, and Kevin K. W. Wang1,2,3*

1Center for Neuroproteomics and Biomarkers Research, Department of Psychiatry, McKnight Brain Institute, Post Office Box 100256, University of Florida, Gainesville, FL 32610, USA.
2Center for Traumatic Brain Injury Studies, Department of Neuroscience, McKnight Brain Institute, Post Office Box 100256, University of Florida, Gainesville, FL 32610, USA.
3Center of Innovative Research, Banyan Biomarkers, Inc., 12085 Research Drive, Alachua, FL 32615, USA.

Gloss: The calpains constitute a class of cellular cysteine proteases that require calcium and are functionally active at neutral pH. In the central nervous system (CNS), controlled activation of calpains may be critical to synaptic function and memory formation. In contrast, physical trauma, or chemical or ischemic insults that lead to a sustained increase in intracellular calcium concentration, may elicit calpain hyperactivation, which is generally associated with severe cellular damage.

*Corresponding authors. E-mail: jingl{at}ufl.edu; kwang{at}banyanbio.com

Citation: J. Liu, M. C. Liu, K. K. W. Wang, Calpain in the CNS: From Synaptic Function to Neurotoxicity. Sci. Signal. 1, re1 (2008).


THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES:
Iron-Induced Oxidative Injury Differentially Regulates PI3K/Akt/GSK3{beta} Pathway in Synaptic Endings from Adult and Aged Rats.
R. M. Uranga, N. M. Giusto, and G. A. Salvador (2009)
Toxicol. Sci. 111, 331-344
   Abstract »    Full Text »    PDF »
Extrasynaptic NMDA Receptors Couple Preferentially to Excitotoxicity via Calpain-Mediated Cleavage of STEP.
J. Xu, P. Kurup, Y. Zhang, S. M. Goebel-Goody, P. H. Wu, A. H. Hawasli, M. L. Baum, J. A. Bibb, and P. J. Lombroso (2009)
J. Neurosci. 29, 9330-9343
   Abstract »    Full Text »    PDF »
Calpain Expression and Activity during Lens Fiber Cell Differentiation.
A. De Maria, Y. Shi, N. M. Kumar, and S. Bassnett (2009)
J. Biol. Chem. 284, 13542-13550
   Abstract »    Full Text »    PDF »
Calpain-Mediated N-Cadherin Proteolytic Processing in Brain Injury.
Y.-N. Jang, Y.-S. Jung, S. H. Lee, C.-H. Moon, C.-H. Kim, and E. J. Baik (2009)
J. Neurosci. 29, 5974-5984
   Abstract »    Full Text »    PDF »

To Advertise     Find Products


Science Signaling. ISSN 1937-9145 (online), 1945-0877 (print). Pre-2008: Science's STKE. ISSN 1525-8882