| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
|
|
|
|||||||
|
|||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Papers In Press, published online ahead of print December 19, 2003
J. Biol. Chem, 10.1074/jbc.M308841200
Submitted on August 11, 2003
Revised on October 30, 2003
Accepted on December 19, 2003
Tumor Genetics and Biology, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Kumamoto 860-8555
Corresponding Author: hsaya{at}gpo.kumamoto-u.ac.jp
Calpains form a superfamily of Ca+2-dependent intracellular cysteine proteases with various isoforms. Two isoforms, 
- and m-calpains, are ubiquitously expressed and known as conventional calpains. It has been previously shown that the mammalian calpains are activated during mitosis by transient increases in cytosolic Ca+2 concentration. However, it is still unknown whether the activation of calpains contributes to particular events in mitosis. With the use of RNA interference (RNAi), we investigated the roles of calpains in mitosis. Cells reduced the levels of m-calpain, but not -calpain, arrested at prometaphase and failed to align their chromosomes at the spindle equator. Specific peptidyl calpain inhibitors also induced aberrant mitosis with chromosome misalignment. Although both m-calpain RNAi and calpain inhibitors affected neither the separation of centrosomes nor the assembly of bipolar spindles, Mad2 was detected on the kinetochores of the misaligned chromosomes, indicating that the prometaphase arrest induced by calpain inhibition is due to activation of the spindle assembly checkpoint. Furthermore, when calpain activity was inhibited in cells having monopolar spindles, chromosomes were clustered adjacent to the centrosome, suggesting that calpain activity is involved in a polar ejection force for metaphase alignment of chromosomes. Based on these findings, we propose that activation of m-calpain during mitosis is required for cells to establish the chromosome alignment by regulating molecules which generate polar ejection force.
CiteULike 
Complore 
Connotea 
Del.icio.us 
Digg 
Reddit 
Technorati What's this?
This article has been cited by other articles:
|
|
 |
|
  W.-T. Chiu, M.-J. Tang, H.-C. Jao, and M.-R. Shen Soft Substrate Up-regulates the Interaction of STIM1 with Store-operated Ca2+ Channels That Lead to Normal Epithelial Cell Apoptosis Mol. Biol. Cell, May 1, 2008; 19(5): 2220 - 2230. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. Honda, F. Masui, N. Kanzawa, T. Tsuchiya, and T. Toyo-oka Specific knockdown of m-calpain blocks myogenesis with cDNA deduced from the corresponding RNAi Am J Physiol Cell Physiol, April 1, 2008; 294(4): C957 - C965. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 B. Helfer, B. C. Boswell, D. Finlay, A. Cipres, K. Vuori, T. Bong Kang, D. Wallach, A. Dorfleutner, J. M. Lahti, D. C. Flynn, et al. Caspase-8 Promotes Cell Motility and Calpain Activity under Nonapoptotic Conditions. Cancer Res., April 15, 2006; 66(8): 4273 - 4278. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 V. S. Golubkov, S. Boyd, A. Y. Savinov, A. V. Chekanov, A. L. Osterman, A. Remacle, D. V. Rozanov, S. J. Doxsey, and A. Y. Strongin Membrane Type-1 Matrix Metalloproteinase (MT1-MMP) Exhibits an Important Intracellular Cleavage Function and Causes Chromosome Instability J. Biol. Chem., July 1, 2005; 280(26): 25079 - 25086. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. Fenech, P. Baghurst, W. Luderer, J. Turner, S. Record, M. Ceppi, and S. Bonassi Low intake of calcium, folate, nicotinic acid, vitamin E, retinol, {beta}-carotene and high intake of pantothenic acid, biotin and riboflavin are significantly associated with increased genome instability--results from a dietary intake and micronucleus index survey in South Australia Carcinogenesis, May 1, 2005; 26(5): 991 - 999. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
| All ASBMB Journals | Molecular and Cellular Proteomics |
| Journal of Lipid Research | ASBMB Today |
