hamlet代写-肿瘤抑制因子

28 10月 hamlet代写-肿瘤抑制因子

本文的内容是肿瘤抑制因子,这种蛋白质的过度活跃形式经常在致癌细胞中发现。例如,在90%的胰腺癌中发现了含有致癌基因的Ras突变。此外,Ras是一种G蛋白,意味着它开始前后转换(cleveland, 2011)。这意味着它有时是活跃的,有时是不活跃的。引起癌症的突变常常改变Ras的结构,使其不能再转变为非活性状态。这使得蛋白质保持在开启状态。本篇hamlet代写文章由英国论文人EducationRen教育网整理,供大家参考阅读。

Such proteins overactive forms are often found within cancer causing cells. For example, Ras mutations with oncogenes have been found in pancreatic cancers of 90 percent. Ras furthermore is a G protein implying that it starts switching front and back (Clevers, 2011). This means that it is sometimes active and other times inactive. Mutations causing cancer often change the structure of Ras so that it is no more able to switch towards its inactive state. This makes the protein to remain in turned on state.
Suppressors of tumour: Cell cycle negative regulators might have less activity within cells of cancer. For example, a protein results in halting the progression of cell cycle as a response to damage of DNA. This might no more have the ability of sensing damage or triggering response. There are genes which normally result in blocking the progress of cell cycle and these are called as suppressors of tumour (Dancey et al., 2012). These suppressors result in preventing cancerous tumours formation when they are performing their role properly and it is possible for tumours to form when these cells mutate in such a manner that they are not able to work anymore.
One of the most essential suppressors of tumor is protein p 53 tumour. It plays an essential role in the DNA damage cellular response. P 53 is such that it primarily acts as the checkpoint for G1 in which it results in blocking the progress of cell cycle as a response to DNA damages and other unflavoured situations (Thangavelu et al., 2012). When the DNA of the cell has any damages, a protein sensor will result in activating the p 53, which in turn halts the G1 checkpoint cell cycle through cell inhibiter production being triggered. Such a pause in turn allows buying some time for repair of DNA which is further dependent over p 53. The second task of this lies in activating the repair enzymes of DNA. If there is fixation of damage, p 53 will result in releasing cells allowing them to continue throughout the cycle of ell. When damage cannot be fixed, the final role is played by p 53 (Cheong et al., 2012). This results in apoptosis being triggered such that DNA damage does not get passed over.

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