Fig 5 - uploaded by Luigi Bagella
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![A schematic representation of the main cdk/cyclin complexes involved in cell cycle control. The passage through the four phases of the cell cycle is regulated by the activities of cdks controlled by the synthesis of the appropriate cyclins during a specific phase of the cell cycle. Cell cycle inhibitory proteins, called cyclin-dependent kinase Inhibitors (CKI), can counteract cdk activity. P15, p16, p21 and p27 represent the main CKIs that specifically prevent accumulated G1-Cdk/Cyclins from acting. The G1-Cdk/Cyclin complexes [(Cdk4(6)/Cyclin D and Cdk2/Cyclin E(A)] control the G1/S checkpoint by the phosphorylation of a variety of proteins. The Rb family proteins represent one key target. Their phosphorylation prevents the binding and inactivation of the E2F transcription factors. The activation of E2Fs allows the transcription of various gene products that are indispensable to trigger S phase.](profile/Luigi-Bagella/publication/224829363/figure/fig3/AS:669074111623172@1536531107106/A-schematic-representation-of-the-main-cdk-cyclin-complexes-involved-in-cell-cycle.png)
A schematic representation of the main cdk/cyclin complexes involved in cell cycle control. The passage through the four phases of the cell cycle is regulated by the activities of cdks controlled by the synthesis of the appropriate cyclins during a specific phase of the cell cycle. Cell cycle inhibitory proteins, called cyclin-dependent kinase Inhibitors (CKI), can counteract cdk activity. P15, p16, p21 and p27 represent the main CKIs that specifically prevent accumulated G1-Cdk/Cyclins from acting. The G1-Cdk/Cyclin complexes [(Cdk4(6)/Cyclin D and Cdk2/Cyclin E(A)] control the G1/S checkpoint by the phosphorylation of a variety of proteins. The Rb family proteins represent one key target. Their phosphorylation prevents the binding and inactivation of the E2F transcription factors. The activation of E2Fs allows the transcription of various gene products that are indispensable to trigger S phase.
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Context 1
... inhibitory actions occur through the interaction and inactivation of all the G1-cdk/cyclin complexes (Besson et al., 2008). In summary, these CKIs can indirectly inhibit the E2F-mediated transcription through the interaction and inhibition of cdk/cyclin complexes that, maintaining the Rb family proteins in a hypophosphorylated state, allow them to sequester the E2F transcription factors ( figure 5). Notwithstanding the wide variety of functions of the pocket proteins is E2F-responsive genes dependent, p130, as well as p107, is able to suppress cell growth through its interaction with two significant cell cycle complexes mentioned above, Cdk2/Cyclin A and Cdk2/Cyclin E ( Zhu et al., 1995;Lacy & Whyte, 1997). ...
