Cyclins provide binding interfaces for substrate targets, substrate specificity. Cyclins bind to CDKs and activate them. Cyclin levels rise and fall corresponding to the part of the cell cycle the cell is in! CAK (CDK activating kinase) adds phosphate to T-loop, enabling CDK to phosphorylate and activate its substrates. WEE1 kinase phosphorylates CDK at a different amino acid and holds it in an inactive state. Cdc25 removes that inactivating phosphate added to CDK by WEE1 and activates it (activating phosphatase). CDK phosphorylates Rb and causes its dissociation from E2F. Rb binds E2F, preventing it from causing over replication, when Rb is phosphorylated, it lets go of E2F. When E2F is active, the cell has committed to the cell cycle. P53 can detect problems during replication and will act as a transcription factor for inhibitors of the cell cycle such as CDKI. It will wait until things are fixed or activate apoptosis if it goes on for too long. CDKs 1,2,4, and six are present in vertebrates. CDK1 is the most important.
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