Thursday, July 18, 2019
The Division of Cells
The main purpose of this base is to explain how the division of carrells is broad(prenominal)ly modulate such that cubicles that fail to pass close to specific stage-based tests cannot advance to the proceeding stages. Basically, the hertz is directly attached to some bioenergetic and biosynthetic demands, and prior to the division process, cell components in the parent cell have to be doubled and later distributed equally to the resulting girl cells following a division process.This do hypothesizes that addition of phosphate moieties to the CDC25C by an enzyme called Adenosine Monophosphate-activated protein kinase acts as a mediator of a metabolous checkpoint that seeks to control cell division specifically at the point where the cells are transitioning from the G2 to the M soma.The research question that is being well-tried in this constitution was more or less the energizing of the protein kinase and how it works to be a high energy sensor that plays a pregnant rol e in cells that lack of the essential bioenergy requirements that do not enter the mitotic phase during the cell division.The most important facet of this experiment in the paper was about the HeLa cells which were subjected to chemicals that are known to activate the enzyme AMPK. Also, the main catabolic processes that are involved to bewilder energy for cells to transition from G1/G2 were descendd by the application of radiochemical approaches, the experiment required to determine if AMPK activation had a hand in preventing mitosis.The results confirmed that activation of this enzyme prevented entry into mitosis.The paper presents a conflicting idea when it comes to the decision making if there is role of mTORC1 in the cell division process, so I believe the weaknesses related to the experimental procedures that they designed, they activated AMPK or some otherwise inactivated mTORC1 in a style that is not clearly proved and so following from this, one cannot really spot if the mitosis regulation was due to AMPK activation of mTORC1 inactivation.If this was my experiment, I would start with two separate setups should be conducted, one with activated AMPK and eliminated CDC25C to check whether there is any influence on mTORC1, and the other set up then go out contain cells activated AMPK and have CDC25C and eliminated mTORC1. The results should then be cross-checked to see if AMPK only affects CDC25C or mTORC1 independently or both at the same time. This will help in the keen determination of the exact gravel of cell cycle regulation when it comes to the cell division phases and stages.
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