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Genes such as proto-oncogenes and tumor suppressor genes code the production of various proteins that aid in the proper progression of the cell cycle, the former encouraging replication and the latter inhibiting it. Proto-oncogenes are part of the formation of cyclins (proteins) and cyclin dependent kinases (CDK enzymes) which are the central controls and regulators of cell cycle checkpoints. Other proto-oncogenes such as SRC and RAS proto-oncogenes also help in communicating growth factor signals to cells, letting them know growth is necessary and stumlating the cell cycle. Proto-oncogenes are normal genes that have the potential to become tumor causing, or oncogenes, if exposed to mutagens and will often code for cyclins that activate CDKs, which trigger continuation of the cell cycles. Tumor Suppressor Genes on the other hand, code for proteins such as p53 that can inhibit the activation of CDK’s in the case of an abnormal cell, pausing the cell cycle and prohibiting the abnormal cell from replicating (Oncogenes).  Firstly, in order to understand the role that these regulators play, it is important to discuss the way the checkpoints operate the cell cycles. Maintenance of cell cycle checkpoints is essential to normal cell replication, as they work as a form of quality control, checking the cell at the checkpoints G1, G2 and M. Checkpoint G1 is present at the transition between the G1 and S phases in interphase, and here the cell is checked for DNA integrity and growth factors, sending it on if it passes the test—otherwise it is sent to G0, a resting phase until passing, or apoptosis. In checkpoint G2 between the G2 and M phase of cell replication, the cell is checked for proper DNA replication and continues or is marked for apoptosis, a programmed cell death that ensures damaged cells cannot replicate. Checkpoint M, or the mitotic checkpoint, which ensures that the sister chromatids are attached to opposite sides of the pole so that they can be spliced correctly (textbook).  At the G1 checkpoint, cyclins and cyclin dependent kinases (CDKs) work together hand in hand in order to put the transition through checkpoints into motion. Essentially, CDKs and cyclins bind and activate cycle-specific target proteins within a cell by phosphorylating, prompting the cell to continue to transition along that part of the cell cycle. If, however, a cell’s genome is damaged, kinases such as ATM/ATR phosphorylate the p53 tumor suppressor gene which in turn will activate CDK inhibitors, pausing the cell cycle and preventing the damaged gene from replicating. The damaged cell will likely be sent to G0 phase, where it will stay until it can be repaired. If the damaged DNA cannot be reformed, it may remain in limbo until apoptosis is triggered by the p53 signal. This process prevents the uninhibited reproduction of damaged cells, which may have mutated genomes that could possibly become cancerous. It is clear therefore, that p53 is essential in maintaining a healthy cell-cycle—were the p53 gene were to be mutated or otherwise incapacitated, the body would have little protection from a rapid accumulation of cancer cells (“Cell cycle regulators”). Another important cell control mechanism is conducted by the c-SRC proto-oncogene, and the RAS proto-oncogene which aid in communicating that a growth factor has triggered cell growth. c-SRC sits just inside the cell membrane and communicates this to the cell, and Genes and proteins can mutate due to numerous factors and mutagens such as ultraviolet radiation exposure and other toxins. For example, if a c-SRC protein or a RAS protein were to be mutated, they could be detected by the cell as an unending on-switch signaling uninhibited growth. RAS oncogenes can also mutate tumor suppressor genes such as p53, rendering them incapable of pausing the cell cycle. Resultantly, the cells could receive a misinterpreted signal and reproduce despite a damaged genome. Furthermore, the growth of cells could occur more frequently and tumors occur when the growth of certain abnormal cells is uninhibited, resulting in the formation of tumors, benign or cancerous. In fact, studies have shown that mutations of p53 are a causal factor to 50% of all cancer cases.  

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