Synthesis of -carbolines as novel CDK4 inhibitors Lab Report

Synthesis of -carbolines as novel CDK4 inhibitors - Lab Report Example Considering the importance of Cyclin-dependent kinases (CDKs), a set of protein kinases, it is essential to explore its mechanism that makes it relevant for the lab process. The kinases aid in regulating the cell cycles, transcription Mrna processing and differentiation of nerve cells. In the function of these kinases, cyclin is crucial considering that it acts as the regulatory protein which binds the CDKs. Consequently, this means that in the absence of cyclin, less kinase activity takes place because of the absence of cyclin-CDK complexes1. CDK4, acting as a member of the cyclin-dependent kinase family, functions as an intrinsic catalyutic protein kinase complex for cell cycle G1 phase progression. D type cyclins and CDK inhibitor are important for the functioning of the kinase since they suppress the action of tumour in causing cell proliferation. The kinase works in phosphorylation of the retinoblastoma gene product thereby helping in preventing the occurring mutation of the genes responsible for the tumuourigenesis of various types of cancer 2. Further, small compouds such as pentacyclic quaternary salt, act as promising factors in the direction for treatment of cancer. The action of the kinase in causing DNA-interchelation can be reduced by ÃŽ ²-carboline which usually acts as a non-planner maintaining the activity of CDK4. Fascaplysin acts as a pentacyclic quaternary salt used as an anti-cancer agent considering its action in suppressing certain leukemia cells in mice. Further, the salt also end up hindering CDK4 leading to arrest of cell cycle in both normal and tumours ncells in the G phase. The hindering process occurs because it binds to theATP pocket of the kinase, resulting to G arrest via a bidentate hydrogen bond donor/acceptor pair. The chain involving phosphorylation of pRb enables the cell to pass through the G1 checkpoint leading to completion of division cycle because of the associated release of E2F proteins.