Transition from G2 to M phase of cell cycle is controlled by
Correct Answer: Cyclin B
Description: Ref Robbins 7/e p290-291 Your Position: Cell Cycle Inhibitor Proteins Cell Cycle Inhibitor Proteins Creat Cell Cycle Inhibitor Proteins The cell cycle is the series of events which regulate the life of the cell. This regulation results from a combination of several signals from different regulatory pathways that are activated in response to specific stimuli. The cell cycle has a central role in controlling cell growth and proliferation. It frequently becomes the target of genetic alteration, the accumulation of which may lead to the deregulation of these ordered events and may be related to the onset of cancer. With the growing understanding of the impoant role of cell cycle regulation in tumor formation and apoptosis, cell cycle inhibitors have been fuher studied in the field of cancer treatment. Cyclin-dependent Kinase (CDK) Inhibitors Progression through the cell cycle is ensured by paicular protein complexes, the cyclin-dependent kinases (CDKs). The CDKs are a family of highly conserved serine/threonine kinases, which share a high homology in a paicular region. CDKs may control the cell cycle by phosphorylating different targets, which may in turn be activated or inactivated. Regulation of CDK/cyclin activity can occur through regulatory proteins, such as CDK Inhibitors (CKIs). The CKIs can inhibit the activity of CDK by associating in vivo with the CDK subunit, the cyclin or the cyclin/CDK complex. This inhibition may occur in different ways, such as inhibition of the CDK kinase activity, interference with CAK mediated CDK activation, or competition with cyclins in binding to the catalytic subunit. The inhibitory process can be carried out by one or a combination of these mechanisms. The expression of these CKIs may be induced by stimuli such as senescence, contact inhibition, extracellular anti-mitogenic factors and cell cycle checkpoints. Their role in controlling cell cycle is crucial. In several forms of cancer, CKIs such as p16 and p27 are mutated. Also, they have been found to be degraded in several types of cancer. Low levels of p27 levels are correlated with poor clinical prognosis. These inhibitors can be upregulated when required, thus blocking the activation of the CDK by a cyclin. This arrests the cell in a paicular pa of the cell cycle until conditions are such that it can continue towards proliferation or, if necessary, be steered towards cell death.
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