Abstract
Centrosome cycle studies reveal promising candidates for anti-cancer drug design.
Highlights
Given the correlation between centrosome number and tumor progression, molecules regulating centrosomal duplication at the G1/S transition have been under considerable scrutiny
CaMKII is likely triggered in response to the periodic calcium oscillations that occur at the G1/S transition and are required for centrosome duplication
Hannak et al employed an RNAi strategy to query the role of Caenorhabditis elegans Aurora A during the first embryonic cell division (J Cell Biol 2001, 155:11091116)
Summary
Given the correlation between centrosome number and tumor progression, molecules regulating centrosomal duplication at the G1/S transition have been under considerable scrutiny. Fisk and Winey recently used a culturebased assay of centrosome duplication to query the relevance of mMps-1p, the mouse orthologue of the Saccharomyces cerevisiae MPS1p protein kinase, a protein known to regulate spindle pole body replication (Cell 2001, 106:95-104). Matsumoto and Maller have demonstrated that, in the context of S-phase-arrested Xenopus extracts, it is calcium/calmodulin-dependent kinase (CaMKII), and not CDK2, that initiates centrosomal duplication (Science 2002, 295:499-502).
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