The dividing life of a cell is called the cell cycle which includes growth, doubling of genetic material, and division into new cells. The cell cycle has 2 subgroups: interphase and mitosis. Interphase refers to “preparing to divide.” The interphase has 3 sub-phases which are; G1, S and G2. On the other hand, there is the G0 phase called quiescent state. In the G0 phase the cells have no division process, the cells only maintain their vital process without growth. Mitosis represents cell division which involves 5 sub-phases; prophase, metaphase, anaphase, telophase and cytokinesis where cytoplasmic division occurs. External signals have an effect on the cell to decide to enter the cell cycle process. Mitogenic growth factors prime cells for active growth and cell division if they are present in sufficient concentration in the cellular environment. But if their concentration in the environment is not sufficient, the cell remains in the G0 phase. The cell is maintained in G0 when the growth inhibitory factors are entities such as TGF-β. Receptor tyrosine kinases, G-coupled receptors, integrins, and nutrient status can be given as examples of 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 the G1 phase. In the mammalian cell, G1 takes 6 to 8 hours. DNA duplication occurs in the 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 Shouldn't Be Banned"? Get an original essay The spindle apparatus can be seen in the G2 phase. At the end of the interphase section, the cells go into mitosis where nuclear and cytoplasmic division occur. Condensation of chromosomes, localization of the centrosome, and disappearance of the nucleolus are found in prophase. During metaphase, chromosomes line the metaphase plate, the nuclear envelope disappears, microtubules attach chromosomes to the kinetochore which interacts with the centromere where two sister chromatids are held together. Sister chromatids attract opposite poles of the cell during anaphase. During telophase, chromatids are decondensed and the nuclear envelope forms for each set of chromatids. After all these steps have occurred, cytoplasmic division called cytokinesis begins. As you can understand, the cell cycle process is long and arduous. Additionally, several diseases, including cancer, occur 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 called the G1 checkpoint, G2 checkpoint, and M checkpoint. At the G1 checkpoint, DNA integrity, size, molecular signaling, and nutrients are checked. If there are no problems, the cell undergoes the S phase. Conversely, if there is a problem, the cell undergoes the G0 phase. DNA integrity and proper DNA replication are checked in the G2 phase. The cell activates the repair system when there is a challenge. If this challenge cannot be repaired, the cell undergoes apoptosis or programmed cell death. This checkpoint is critical to preventing cancer from forming. The M checkpoint controls the attachment of the chromosome to the spindle at the metaphase plate. As mentioned above, the cell makes the decision about growth and quiescence. This decision is linked to external signals. Anti-mitogenic factors such as TGF-β which has an inhibitory effect on growth. On the other hand, growth factorsmitogens cause the cell to grow. At the restriction point, which is located at the end of G2, the cell decides to move into the G0 or S phase. The cell cycle process is regulated by several 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 the cell cycle. Cyclin-dependent kinases that are inactive alone are responsible for activating targets via phosphorylation while active with cyclins. CDKs participate in serine/threonine kinases with which they interact with growth factor receptor and 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 the 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 transition into S phase by phosphorylation of appropriate protein substrates. CDK2 associates with A-type cyclins (dissociates E-type cyclins) in S phase and allows S phase to progress. A-type cyclins associate with CDC2 or CDK1 later in S phase. As the cell undergoes G2 phase, CDC2 makes a deal with B-type cyclins that trigger mitosis events such as prophase, metaphase, anaphase, and telophase. External mitogens such as Wnts via β-catenin and transcription factor Tcf/Lef, cytokines via STAT, and various ligands via NF-κB increase cyclinD1 leading to the cell cycle. CDK inhibitors (CDKIs) are important proteins that have a negative effect on the cell cycle. INK4 (CDK4 inhibitors) target CDK4 and CDK6 with no 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 referred to as p21Waf1), p27Kip1, and p57Kip2. When TGF-β is present in the cell's environment, p15INK4b is activated and 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 DNA damage is repaired. Surprisingly, there is a different process found in p21Cip1 and p27Kip1. They have a role in the inhibition of cyclin E-CDK2, on the other hand they stimulate the formation of the cyclin D-CDK4/6 complex. The 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 degradation of cyclin M and destruction of the cohesin protein that holds sister chromatids together, so APC/C allows separation of chromotids in anaphase through the opposite site. APC/C has a different working process than CDKs. It adds ubiquitin to its target which causes protein degradation by the proteasome. The cohesin degradation pathway begins with the addition of ubiquitin to securin which binds the separase enzyme to inactivate separase. When securin is ubiquitinated, it is destroyed by the proteasome and separase becomes active. Active separase plays a role in the degradation of cohesion that causes separation of sister chromatids. p53 is another protein known as a tumor suppressor. p53 triggers the formation of CDKIs, which destroy cyclin/CDK complexes, when there is DNA damage. Additionally, it activates DNA repair enzymes. If this damage cannot be resolved, P53 acts as a stimulus for programmed cell death. pRb also functions as a tumor suppressor. pRb binds the E2F transcription factor, il9876.2018.1657