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| Type |
Poster Presentation |
| Area |
Life Chemistry |
| Room No. |
Exhibition Hall 2+3 |
| Time |
10월 19일 (목요일) 11:00~12:30 |
| Code |
BIO.P-249 |
| Subject |
Misfolded Z-type α1-Antitrypsin Proteins Induce Oxidative Stress |
| Authors |
Hana Im*, JAEYEON LIM
Department of Integrative Bioscience and Biotechnology, Sejong University, Korea
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| Abstract |
Protein misfolding and aggregation is associated with various human degenerative diseases, including type II diabetes, Alzheimer’s, Huntington’s, and Parkinson’s diseases. Accumulation of misfolded Z-type variant of human α1-antitrypsin protein in the ER leads to persistent ER stress and subsequent cell death, leading to liver cirrhosis. A Saccharomyces cerevisiae ORF-deletion library was screened for the response elements to accumulation of misfolded Z-type α1-antitrypsin protein. Several deletion mutants of redox regulator genes aggravated Z-type α1-antitrypsin-induced cytotoxicity. We have also shown that overexpression of Z-type α1-antitrypsin caused cellular oxidative stress by dichlorofluorescein assays. Z-type α1-antitrypsin-producing cells became vulnerable to further oxidative challenges with low concentrations of hydrogen peroxide. Treatment with antioxidant chemicals, such as ascorbic acid, N-acetylcysteine, or butylated hydroxyanisole protected yeast cells from Z-type α1-antitrypsin-induced cytotoxicity. Our data all together provide further insight on cell defense mechanism against protein folding problems, and suggest future therapeutic applications.
This work was supported by grants from the National Research Foundation of Korea (KRF-2015R1D1A1 A01058206). |
| E-mail |
hanaim@sejong.ac.kr |
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120th General Meeting of the KCS