Yeast cells rely on several signaling pathways for cell cycle regulation. These include the PKA, TOR, and ribosome biogenesis pathways. These pathways regulate the cell cycle by regulating ribosome biogenesis and translational activity. They can also regulate cell growth and differentiation.
The cell cycle is a critical process in cancer progression. The breakdown of this process can cause cancer by altering gene sequences and disrupting regulatory components. Studying the molecular details of proteins such as CDK2 can help discover new therapeutic targets. For example, recent high-resolution structures of CDK2 and p53 may reveal potential therapeutic targets.
Cell cycle progression may be correlated with cell size. For example, a larger cell will move faster through the G1 and G2 phases of the cell cycle. A smaller cell will move slowly through these phases. Interestingly, the location of these checkpoints differs among different species and cell types.
Moreover, many cancer-related genes are proto-oncogenes. These genes code for proteins that regulate the cell cycle. A mutated copy of a proto-oncogene causes cancer by overriding cell cycle checkpoints. In these circumstances, the cell may divide uncontrollably.
Cyclin-dependent kinases (CDK) are serine-threonine-protein kinases that phosphorylate key substrates involved in DNA synthesis and mitotic progression. CDK activity is tightly regulated at the synthesis and proteolysis levels. Small inhibitory proteins can block phosphorylation of CDK catalytic subunits, thus suppressing their activity.
Cell cycle regulation is essential to the growth and development of all cells. Without it, cells would not reproduce properly, resulting in uncontrolled division and cancer. Moreover, it can result in a disproportionate number of cells in an individual’s body. Hence, cell cycle regulation is necessary to prevent this uncontrolled cell division.
There are two types of supervisory cell cycle regulation: checkpoint control and CDK inhibition. Cells use checkpoints to detect flaws in critical events like DNA replication and chromosome segregation. Using this information, checkpoints can delay cycle progression until the threat of mutation has been eliminated.