The dividing life of a cell is called cell cycle which includes growth, doubling of genetic material and division into new cells. The cell cycle includes 2 subgroups: interphase and mitosis. Interphase refers to “preparing to divide.” Interphase has 3 sub-phases which are: G1, S and G2. On the other hand, there is a G0 phase called resting state. In G0 phase, cells have no division process, cells only maintain their living process without growth. Mitosis represents cell division which has 5 sub-phases; prophase, metaphase, anaphase, telophase and cytokinesis where cytoplasmic division occurs. External signals have an effect on the cell to decide whether to enter the cell cycle process. Mitogenic growth factors trigger active growth and cell division of cells if they are in sufficient concentration in the cellular environment. But if their concentration in the environment is not sufficient, the cell remains in phase G0. The cell maintains at G0 when the growth inhibitory factors are entities such as TGF-β. Tyrosine kinase receptors, G-coupled receptors, integrins, and nutritional status can be given as examples for other external signals. As mentioned above, G1 is one of the subphases of interphase in which the cell decides whether to grow or quiescence with differentiation. Cell growth occurs and biosynthesis increases in G1 phase. In mammalian cells, G1 takes 6 to 8 hours. DNA duplication takes place in S phase. The centrosome also duplicates and the amount of histone proteins increases. Say no to plagiarism. Get a tailor-made essay on “Why Violent Video Games Should Not Be Banned”? Get the original essay. The pin device can be seen at phase G2. After the end of the interphase section, cells enter mitosis where nuclear and cytoplasmic division occur. Chromosome condensation, localization of centrosomes and disappearance of the nucleolus are localized in prophase. During metaphase, the chromosomes align the metaphase plate, the nuclear envelope disappears, the microtubules attach the chromosomes to the kinetochore which interacts with the centromere where two sister chromatids are held together. Sister chromatids pull opposite poles of the cell during anaphase. During telophase, the chromatids are decondensed and a nuclear envelope forms for each set of chromatids. After all these steps, the cytoplasmic division called cytokinesis begins. As can be understood, the cell cycle process is long and arduous. Additionally, different diseases arise, including cancer, if there is a problem at any stage of the cell cycle. Therefore, cells have checkpoints where the cell cycle is controlled. These checkpoints are named checkpoint G1, checkpoint G2 and checkpoint M. At checkpoint G1, DNA integrity, size, molecular signal and nutrients are checked. If there is no problem, the cell goes into phase S. On the other hand, if there is a problem, the cell goes through phase G0. DNA integrity and proper DNA replication are verified during the G2 phase. The cell activates the repair system in the event of a challenge. If this problem cannot be repaired, the cell undergoes apoptosis or programmed cell death. This checkpoint is crucial for preventing cancer formation. The M checkpoint controls chromosome spindle attachment at the metaphase plate. As mentioned above, the cell makes a decision regardingits growth and its tranquility. This decision is linked to external signals. Anti-mitogenic factors such as TGF-β which have a growth inhibitory effect. On the other hand, mitogenic growth factors induce cell growth. At the restriction point, located late G2, the cell decides to move to G0 or S phase. The cell cycle process is regulated by different genes and proteins. Cyclin, cyclin-dependent kinases (CDKs), CDK inhibitors, apoptosis-promoting complex/cyclosome (APC/C), p53, and pRb are the most common areas of research when the topic is cell cycle . Cyclin-dependent kinases, which are inactive by themselves, are responsible for activating targets via phosphorylation while they are active with cyclins. CDKs participate in serine/threonine kinases that interact with growth factor receptor and with a non-receptor kinase molecule. Cyclins play an important role in the catalytic activation and recognition capacity of CDKs during the binding process of their protein substrate. In G1 phase, CDK4 and CDK6 are activated by D-type cyclins (D1, D2 and D3). When the R point at the end of G2 is passed, E-type cyclins interact with CDK2. This process allows the cell to undergo S phase by phosphorylation of appropriate protein substrates. CDK2 associates with A-type cyclins (dissociates E-type cyclins) in S phase and allows progression into S phase. A-type cyclins associate with CDC2 or CDK1 later in S phase. When the cell passes G2 phase, CDC2 enters into an agreement with B-type cyclins that trigger mitotic events such as prophase, metaphase, anaphase, and telophase. External mitogens such as Wnts via β-catenin and transcription factor Tcf/Lef, cytokine via STAT, and various ligands via NF-κB increase cyclinD1, which leads to the cell cycle. CDK inhibitors (CDKIs) are important proteins that have a negative effect on the cell cycle. INK4 (CDK4 inhibitors) targets CDK4 and CDK6 without any effect on CDC2 and CDK4. INK4 inhibitors are p16INK4a, p15INK4b, p18INK4c, p19INK4d. All other cyclin-CDK complexes (E-CDK2, A-CDK2, A-CDC2, B-CDC2) are inhibited by p21Cip1 (or named p21Waf1), p27Kip1 and p57Kip2. When TGF-β is present in the cell's environment, this triggers p15INK4b which blocks cyclin D-CDK4/6 complexes. For this reason, the cell does not reach the R point at the end of G2 without cyclin D/CDK4/6. p21Cip1 used during the damage repair system inhibits cyclin E-CDK2 complexes until the DNA damage is repaired. Surprisingly, there is a different process in p21Cip1 and p27Kip1. They play a role in the inhibition of cyclin E-CDK2, but they stimulate the formation of the cyclin D-CDK4/6 complex. Binding of cyclin M to CDKs promotes mitosis of the cell. The other protein is the anaphase-promoting complex/cyclosome (APC/C). This complex causes the degradation of cyclin M and destruction of the cohesin protein that holds sister chromatids together, so that APC/C allows separation of chromotids in anaphase via the opposite site. APC/C has a different work process than CDKs. It adds ubiquitin to its target, which causes the proteins to be broken down by the proteasome. The cohesin degradation pathway begins the addition of ubiquitin to securin which binds to the separase enzyme to inactivate the separase. When securin is ubiquitinated, it is destroyed by the proteasome and separase becomes active. Active separase plays a role in the degradation of cohesin which results in separation of sister chromatids. p53 is another protein known as a tumor suppressor. p53 triggers the9876.2018.1657