alexa Functional Study Of The PEG10 Protease | 66900
ISSN: 2329-6577

Biological Systems: Open Access
Open Access

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JOINT EVENT on 2nd International Conference on Bioscience and 5th International Conference on Integrative Biology

Maria Golda, Mohamed Mahdi, Janos Andras Motyan and Jozsef Tozser
University of Debrecen, Hungary
Posters & Accepted Abstracts: Biol Syst Open Access
DOI: 10.4172/2329-6577-C1-009
Abstract
The Paternally Expressed Gene10 (PEG10) is a retrotransposon-derived imprinted gene in the human genome. Mutation in the coding sequence of the gene is lethal in embryological age due to defects of placental development. PEG10 has been implicated in the development of pancreatic cancer, embryonic kidney Wilms tumor, hepatocellular carcinoma and lymphocytic leukemia, suppressing apoptosis. PEG10 mRNA encodes for two protein isoforms, the reading frame 1 (PEG10- RF1) Gag-like protein and reading frames 1 and 2 (PEG10- RF1/2) Gag-Pol-like polyprotein, which is translated by a typical retroviral frameshift mechanism. The RF2 protein contains an -Asp-Ser-Gly- sequence which corresponds to the consensus active-site motif of retroviral aspartic proteases. We hypothesized that activity of this protease might be required for the strongly observed oncogenic effect of PEG10, in inducing cellular proliferation and suppressing apoptosis. Therefore, PEG10 protease (PR) may be regarded as a chemotherapeutic target. In order to investigate PEG10 PR, the amplified wild-type RF1/2 sequence was cloned into a pQE-TriSystem expression vector. We have also created an inactive PR mutant RF1/2 (D370A) to analyze the activity of the PR. To study the implication of PEG10 PR in cellular proliferation and viability, RF1/2 plasmids containing either a wild-type PEG10 PR or a D370A mutant were transfected into HEK mammalian cells. Our results indicate that overexpression of PEG10 PR may indeed result in the induction of cellular proliferation. Interestingly, when cell viability was assessed, transfection with wild-type PEG10 had a detrimental effect on cell viability.
Biography

Mária Golda earned her Master’s degree in Molecular Biology from the Faculty of Medicine, University of Debrecen. She has done her PhD under the supervision of Dr. József Tőzsér in Retroviral Biochemistry Laboratory (LRB), in the Department of Biochemistry and Molecular Biology (University of Debrecen).

Email: [email protected]

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