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Cell cycle
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== Checkpoints == {{Main|Cell cycle checkpoint}} [[Cell cycle checkpoint]]s are used by the cell to monitor and regulate the progress of the cell cycle.<ref>{{cite journal | vauthors = Elledge SJ | title = Cell cycle checkpoints: preventing an identity crisis | journal = Science | volume = 274 | issue = 5293 | pages = 1664β1672 | date = December 1996 | pmid = 8939848 | doi = 10.1126/science.274.5293.1664 | s2cid = 39235426 | bibcode = 1996Sci...274.1664E }}</ref> Checkpoints prevent cell cycle progression at specific points, allowing verification of necessary phase processes and repair of [[DNA damage]]. The cell cannot proceed to the next phase until checkpoint requirements have been met. Checkpoints typically consist of a network of regulatory proteins that monitor and dictate the progression of the cell through the different stages of the cell cycle. [[File:Control Mechanism of Cell Cycle Progression.jpg|thumb|550x550px|Overview of the Cell Cycle checkpoints, visual reference of what it does and where it happens.]] It is estimated that in normal human cells about 1% of [[DNA damage (naturally occurring)|single-strand DNA damages]] are converted to about 50 endogenous DNA double-strand breaks per cell per cell cycle.<ref name = Vilenchik2003>{{cite journal | vauthors = Vilenchik MM, Knudson AG | title = Endogenous DNA double-strand breaks: production, fidelity of repair, and induction of cancer | journal = Proceedings of the National Academy of Sciences of the United States of America | volume = 100 | issue = 22 | pages = 12871β12876 | date = October 2003 | pmid = 14566050 | pmc = 240711 | doi = 10.1073/pnas.2135498100 | doi-access = free | bibcode = 2003PNAS..10012871V }}</ref> Although such double-strand breaks are usually [[DNA repair|repaired]] with high fidelity, errors in their repair are considered to contribute significantly to the rate of cancer in humans.<ref name = Vilenchik2003/> There are several checkpoints to ensure that damaged or incomplete DNA is not passed on to daughter cells. Three main checkpoints exist: the G<sub>1</sub>/S checkpoint, the G<sub>2</sub>/M checkpoint and the metaphase (mitotic) checkpoint. Another checkpoint is the Go checkpoint, in which the cells are checked for maturity. If the cells fail to pass this checkpoint by not being ready yet, they will be discarded from dividing. G<sub>1</sub>/S transition is a rate-limiting step in the cell cycle and is also known as [[restriction point]].<ref name="Robbins"/> This is where the cell checks whether it has enough raw materials to fully replicate its DNA (nucleotide bases, DNA synthase, chromatin, etc.). An unhealthy or malnourished cell will get stuck at this checkpoint. The G<sub>2</sub>/M checkpoint is where the cell ensures that it has enough cytoplasm and phospholipids for two daughter cells. But sometimes more importantly, it checks to see if it is the right time to replicate. There are some situations where many cells need to all replicate simultaneously (for example, a growing embryo should have a symmetric cell distribution until it reaches the mid-blastula transition). This is done by controlling the G<sub>2</sub>/M checkpoint. The metaphase checkpoint is a fairly minor checkpoint, in that once a cell is in metaphase, it has committed to undergoing mitosis. However that's not to say it isn't important. In this checkpoint, the cell checks to ensure that the spindle has formed and that all of the chromosomes are aligned at the spindle equator before anaphase begins.<ref>{{cite journal | vauthors = LeMaire-Adkins R, Radke K, Hunt PA | title = Lack of checkpoint control at the metaphase/anaphase transition: a mechanism of meiotic nondisjunction in mammalian females | journal = The Journal of Cell Biology | volume = 139 | issue = 7 | pages = 1611β1619 | date = December 1997 | pmid = 9412457 | pmc = 2132649 | doi = 10.1083/jcb.139.7.1611 }}</ref> While these are the three "main" checkpoints, not all cells have to pass through each of these checkpoints in this order to replicate. Many types of cancer are caused by mutations that allow the cells to speed through the various checkpoints or even skip them altogether. Going from S to M to S phase almost consecutively. Because these cells have lost their checkpoints, any DNA mutations that may have occurred are disregarded and passed on to the daughter cells. This is one reason why cancer cells have a tendency to exponentially acquire mutations. Aside from cancer cells, many fully differentiated cell types no longer replicate so they leave the cell cycle and stay in G<sub>0</sub> until their death. Thus removing the need for cellular checkpoints. An alternative model of the cell cycle response to DNA damage has also been proposed, known as the [[postreplication checkpoint]]. Checkpoint regulation plays an important role in an organism's development. In sexual reproduction, when egg fertilization occurs, when the sperm binds to the egg, it releases signalling factors that notify the egg that it has been fertilized. Among other things, this induces the now fertilized oocyte to return from its previously dormant, G<sub>0</sub>, state back into the cell cycle and on to mitotic replication and division. [[p53]] plays an important role in triggering the control mechanisms at both G<sub>1</sub>/S and G<sub>2</sub>/M checkpoints. In addition to p53, checkpoint regulators are being heavily researched for their roles in cancer growth and proliferation.
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