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Annotated Bibliography "Primary Information of P53 Gene." Bioinformatics Organization. Bioinformatics Organization, Inc. Web. 1 Oct. 2015. The people that wrote this article are a group or bioinformatics researches that conduct many research projects. The intended audience is people who would like to know more about what the p53 does and a more in depth description of how the protein and gene interact with other parts of the cell. This information us very useful because it tells me what other proteins this protein interacts with and a simplified explanation of these interactions. I can now search for specific information about the interactions between the proteins. This source is not very indepth; it offers an introduction to the p53 gene and everything it does. A potential application of this source to my project would be researching the specifics of the interactions and see if there were places where errors are prone to lead to mutations. I found this source searching for an introduction to everything the p53 gene does in Google. Ute, M., & Oleksi, P. (2003). The MDM2-p53 Interaction. Molecular Cancer Research, 1, 10011008. The people that wrote this are researchers work at a university. They work in the Pathology Department. The intended audience is definitely a scientific community that has a fair amount of knowledge of the subject matter. The information is very useful because it discusses many specific interactions between the p53 protein and the MDM2 protein. This could be applied to my project because since MDM2 regulates p53, there might be a way for MDM2 to force the p53 protein to be disposed. I found this on Google Scholar. Muller, P. A. J., & Vousden, K. H. (2013). p53 mutations in cancer. Nature Cell Biology, 15(1), 2+. The people that wrote this research are researchers of cell biology – the journal name is Nature Cell Biology. The intended audience is people who have a solid understanding of cells and all the organelles within the cells. This information is very useful because many cancerous cells are cancerous due to a mutated p53 gene. If we can find out the mutations and the source of mutations, we might be able to fid something that could prevent certain mutations from happening. I found this source using Google scholar and searched for articles discussing p53 mutations. "The P53 Tumor Suppressor Protein." National Center for Biotechnology Information. National Center for Biotechnology Information. Web. 1 Oct. 2015. This article was on the National Center for Biotechnology Information and was an advanced introduction to thep53 gene. This intended for people that are beginning their research about the p53 gene. This was very useful because the article included an image of the amino acids that were most likely to be mutated – they were the ones that allowed the gene to bind to the DNA. I found this using a Google web search of p53 mutations. Levine, A. J., Rajagopal, G., Hu, W., & Feng, Z. (2008). The tumor suppressor p53: Cancer and aging. Cell Cycle, 7(7), 842-847. doi:10.4161/cc.7.7.5657 This article was published in a journal and meant for the scientific community. This article was very useful because it talked about the relationship between p53 and aging. This could be applied to my research to find differences between young and old population that cause the decline in p53 proteins. This source confirmed that cancer is an elderly disease – p53 functions decline as age progresses – that is why exponentially more people in the last quarter of their life have more cancer. I found this using the WPI database search. Chen, F., Wang, W., & El-Deiry, W. S. (2010). Current strategies to target p53 in cancer. Biochemical Pharmacology, 80(5), 724-730. doi:10.1016/j.bcp.2010.04.031 This article was published by researchers at a university. This article was meant for those who had a very solid understanding of the subject at hand. This article was useful because it provided an overview of attempt to fix the p53 gene to prevent/stop cancer. Maybe I can find flaws or errors with their methods and see what happens if you fix them – this will be an important part because it provides in-depth information about past attempt to target and change the gene. Brachmann, R. K., Yu, K., Eby, Y., Pavletich, N. P., & Boeke, J. D. (1998). Genetic selection of intragenic suppressor mutations that reverse the effect of common p53 cancer mutations. The EMBOJournal, 17(7), 1847-1859. doi:10.1093/emboj/17.7.1847 This article was published by researchers at their respective University’s Department of Medicine. This article was meant for those who had a very solid understanding of the subject at hand. This was somewhat useful to my project because it talks about how when wild type p53s are in the cell, it serves as good cancer therapy. I believe they were looking for mutations that could overcome the negative effects of a mutant p53. This was found using the WPI database. Zhen, S., Hua, L., Takahashi, Y., Narita, S., Liu, Y., & Li, Y. (2014). In vitro and in vivo growth suppression of human papillomavirus 16-positive cervical cancer cells by CRISPR/Cas9. Biochemical and Biophysical Research Communications, 450(4), 1422-1426. doi:10.1016/j.bbrc.2014.07.014 This article was published by researchers at various institutes from Asia. This article was meant for those who had a very solid understanding of the subject at hand. This was very useful because my initial idea was very similar to their project. I’m pretty sure that they are the same thing. I want to fix the mutation in the p53 gene, while their project changed multiple oncogenes that lead to increase in p53. This was found using the WPI database. Wang, Z., & Sun, Y. (2010). Targeting p53 for novel anticancer therapy. Translational Oncology, 3(1), 112. doi:10.1593/tlo.09250 This article was written by researchers at various institutes. This article was meant for those who had a very solid understanding of the subject at hand. This helps out my project because I found out that I should look more into wild type p53 and how it is different from the other two kinds (normal and mutant). I found this source of a Google scholar search. Fuster, J. J., Sanz-González, S. M., Moll, U. M., & Andrés, V. (2007). Classic and novel roles of p53: Prospects for anticancer therapy. Trends in Molecular Medicine, 13(5), 192-199. doi:10.1016/j.molmed.2007.03.002 This article was written by research experts in the fields of biology and pathology. This was meant for someone who knows the information well. This was important because it brought me to consider whether too much p53 would kill the organism – too much of the protein leads to accelerated aging. I found this off WPI’s database.