Difference between revisions of "Part:BBa K4251024"

 
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PDRG1
 
PDRG1
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== Contribution==
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The gene p53 and DNA-damage regulated 1 (PDRG1) was first cloned in 2003 as a small molecule that affects the cellular response to genotoxic stress. An increasing number of studies have confirmed PDRG1 as a tumor marker; the expression of PDRG1 is elevated in a variety of tumor tissues, such as colorectal, ovarian, lung, breast, and endometrial cancers.
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== Engineering==
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Data Downloading and annotation
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The aim of this project is to screen for target genes that can reverse TMZ drug resistance during the treatment of gliomas. Therefore, the public dataset GSE199689 related to TMZ resistance was obtained by screening in the GEO database. This dataset includes two cell lines, U87 (TMZ-sensitive) and U87TR (TMZ-resistant), each with three biological repeats. the biological repeats of U87 are the biological replicates of U87TR are GSM5981756, GSM5981757, and GSM5981758. Using this dataset, the differences between the two cell lines were analyzed and the target genes associated with TMZ resistance were expected to be found. We download the probe and annotated the genes with AnnoProbe. We analyzed the data with R.
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The genes that were significantly up- and down-regulated in the differential genes were screened separately and the expression amounts were observed in each sample. We can see the difference in the expression of differential genes between the two groups (Figure 1).
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[[File:T--SubCat Shanghai--BBa K4251024-figure1.png|500px|thumb|center|Figure 1. the difference in expression of differential genes between the two groups]]
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==Reference==
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1. Lee, S. Y. (2016, May 11). Temozolomide resistance in glioblastoma multiforme. Genes & Diseases. Retrieved July 26, 2022, from https://www.sciencedirect.com/science/article/pii/S2352304216300162
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2. Jiapaer, S., Furuta, T., Tanaka, S., Kitabayashi, T., & Nakada, M. (2018, October 15). Potential strategies overcoming the temozolomide resistance for glioblastoma. Neurologia medico-chirurgica. Retrieved July 26, 2022, from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6186761/
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3. Kato, T., Natsume, A., Toda, H., Iwamizu, H., Sugita, T., Hachisu, R., Watanabe, R., Yuki, K., Motomura, K., Bankiewicz, K., & Wakabayashi, T. (2010, June 3). Efficient delivery of liposome-mediated MGMT-Sirna reinforces the cytotoxity of temozolomide in GBM-initiating cells. Nature News. Retrieved July 26, 2022, from https://www.nature.com/articles/gt201088
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<!-- Add more about the biology of this part here
 
<!-- Add more about the biology of this part here

Revision as of 09:10, 26 September 2022


PDRG1

PDRG1

Contribution

The gene p53 and DNA-damage regulated 1 (PDRG1) was first cloned in 2003 as a small molecule that affects the cellular response to genotoxic stress. An increasing number of studies have confirmed PDRG1 as a tumor marker; the expression of PDRG1 is elevated in a variety of tumor tissues, such as colorectal, ovarian, lung, breast, and endometrial cancers.

Engineering

Data Downloading and annotation The aim of this project is to screen for target genes that can reverse TMZ drug resistance during the treatment of gliomas. Therefore, the public dataset GSE199689 related to TMZ resistance was obtained by screening in the GEO database. This dataset includes two cell lines, U87 (TMZ-sensitive) and U87TR (TMZ-resistant), each with three biological repeats. the biological repeats of U87 are the biological replicates of U87TR are GSM5981756, GSM5981757, and GSM5981758. Using this dataset, the differences between the two cell lines were analyzed and the target genes associated with TMZ resistance were expected to be found. We download the probe and annotated the genes with AnnoProbe. We analyzed the data with R. The genes that were significantly up- and down-regulated in the differential genes were screened separately and the expression amounts were observed in each sample. We can see the difference in the expression of differential genes between the two groups (Figure 1).

Figure 1. the difference in expression of differential genes between the two groups

Reference

1. Lee, S. Y. (2016, May 11). Temozolomide resistance in glioblastoma multiforme. Genes & Diseases. Retrieved July 26, 2022, from https://www.sciencedirect.com/science/article/pii/S2352304216300162

2. Jiapaer, S., Furuta, T., Tanaka, S., Kitabayashi, T., & Nakada, M. (2018, October 15). Potential strategies overcoming the temozolomide resistance for glioblastoma. Neurologia medico-chirurgica. Retrieved July 26, 2022, from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6186761/

3. Kato, T., Natsume, A., Toda, H., Iwamizu, H., Sugita, T., Hachisu, R., Watanabe, R., Yuki, K., Motomura, K., Bankiewicz, K., & Wakabayashi, T. (2010, June 3). Efficient delivery of liposome-mediated MGMT-Sirna reinforces the cytotoxity of temozolomide in GBM-initiating cells. Nature News. Retrieved July 26, 2022, from https://www.nature.com/articles/gt201088


Sequence and Features


Assembly Compatibility:
  • 10
    INCOMPATIBLE WITH RFC[10]
    Illegal EcoRI site found at 1946
    Illegal SpeI site found at 1343
    Illegal PstI site found at 224
    Illegal PstI site found at 1820
  • 12
    INCOMPATIBLE WITH RFC[12]
    Illegal EcoRI site found at 1946
    Illegal SpeI site found at 1343
    Illegal PstI site found at 224
    Illegal PstI site found at 1820
  • 21
    INCOMPATIBLE WITH RFC[21]
    Illegal EcoRI site found at 1946
    Illegal BglII site found at 713
  • 23
    INCOMPATIBLE WITH RFC[23]
    Illegal EcoRI site found at 1946
    Illegal SpeI site found at 1343
    Illegal PstI site found at 224
    Illegal PstI site found at 1820
  • 25
    INCOMPATIBLE WITH RFC[25]
    Illegal EcoRI site found at 1946
    Illegal SpeI site found at 1343
    Illegal PstI site found at 224
    Illegal PstI site found at 1820
  • 1000
    COMPATIBLE WITH RFC[1000]