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Co-expression of S. pombe Csk1 and Cdk1 in insect cells likewise generated monomeric Cdk1 that was phosphorylated on Thr167 and could be activated by cyclin in a single step in vitro [15].
Cell cycle progression is governed by cdks, which are activated by cyclin binding [ 20, 21] and inhibited by the cdk inhibitors [ 22, 23].
Cell cycle progression is governed by cyclin dependent kinases (CDKs) that are activated by cyclin binding and inhibited by CDK inhibitors [ 1].
Pre-RCs are activated by cyclin dependent kinases (CDK) and the Cdc7/ASK kinase, leading to recruitment of elongation factors, Cdc45, DNA polymerases and RPA to origins (Masai and Arai, 2002; Nishitani and Lygerou, 2002).
Cell cycle progression is controlled by cyclin-dependent kinases (CDKs) that are activated by cyclin binding (Sherr, 1994; Morgan, 1995) and inhibited by CDK inhibitors (CDKIs) (Reed et al, 1994; Sherr and Roberts, 1999).
Accumulating evidence that inhibiting the activity of CDKs may be an effective therapy in cancers, including breast cancer, led to the development of small molecules that specifically target subgroups of CDKs, including CDK4 and CDK6, the kinases activated by cyclin D1 [ 4].
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In mammalian cells, progression through the different phases of the cell cycle is regulated by the activity of a series of cyclin-dependent kinases (CDKs) that are activated by cyclins, their regulatory subunits.
These pre-replicative complexes (pre-RCs) are activated by cyclin-dependent kinases and DBF4/CDC7 kinase.
At the G1-S transition pre-RCs are activated by cyclin-dependent kinases (CDKs) and Cdc7/ASK kinase, resulting in recruitment of additional initiation factors and DNA polymerase α-primase to the origin, unwinding of the DNA helix, and initiation of DNA synthesis (Machida et al, 2005).
Cell cycle progression is mostly governed by Cdks, which are activated by Cyclins binding and inhibited by the Cdk inhibitors.
Logically, prior to starting the autoactivation loop, a small amount of cyclin B-Cdk1 should be activated by the cyclin B-Cdk1-independent, putative initial activator (Fig. 4b).
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