Download Annotated Bibliography "Primary Information of P53 Gene

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.