AnaSpec Introduces New Z-Fish™ Antibodies for Cell Cycle Control Research
Product News Aug 14, 2009
Cell proliferation is tightly controlled by cyclin dependent kinases (CDKs) that function sequentially during cell cycle. These kinases phosphorylate and thereby regulate key substrates involved in cell cycle progression1. The regulation of CDKs involves interaction with additional proteins and post-translational modifications. Essential positive regulators of CDKs are the cyclins, regulatory subunits of cyclin/CDK kinase complexes that are expressed periodically during the cell cycle. Furthermore, CDKs are controlled by phosphorylation that either stimulates or represses catalytic activity2. CDK inhibitors (CKIs) have been shown to interact with distinct cyclin/CDK complexes, thereby interfering with their catalytic activity3. Induction of the proto-oncogene cyclin D1, and its binding to CDK4 or CDK6, is a rate-limiting event during cell-cycle progression through G1 phase. Some studies suggested that cyclin D1 also has CDK-independent functions4. Studies in zebrafish model show that cyclin D1 is upregulated by meis1. Cyclin D1 also controls several development processes and in some way, carcinogenesis5. p27KIP1 (p27) is a CKI that was originally identified as a protein capable of inhibiting G1 cyclin/CDK complexes. p27 was discovered as a protein whose expression is induced by different growth inhibitory agents, including tumor growth factor beta6–9. Thus, p27 links proliferative and anti-proliferative signals and controls the transition from the G1 into the S phase of the cell cycle.