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논문 기본 정보

자료유형
학술저널
저자정보
Yun-Sook Lim (Jeonbuk National University) Men T.N. Nguyen (Hallym University) Thuy X. Pham (Jeonbuk National University) Trang T.X. Huynh (Jeonbuk National University) Eun-Mee Park (National Institute of Health) Dong Hwa Choi (Gyeonggido Business & Science Accelerator) Sang Min Kang (Jeonbuk National University) Dongseob Tark (Jeonbuk National University) Soon B. Hwang (Jeonbuk National University)
저널정보
한국분자세포생물학회 Molecules and Cells Molecules and Cells 제45권 제3호
발행연도
2022.3
수록면
148 - 157 (10page)
DOI
10.14348/molcells.2021.0167

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Hepatitis C virus (HCV) is a major cause of chronic liver disease and is highly dependent on cellular proteins for viral propagation. Using protein microarray analysis, we identified 90 cellular proteins as HCV nonstructural 5A (NS5A) interacting partners, and selected telomere length regulation protein (TEN1) for further study. TEN1 forms a heterotrimeric complex with CTC and STN1, which is essential for telomere protection and maintenance. Telomere length decreases in patients with active HCV, chronic liver disease, and hepatocellular carcinoma. However, the molecular mechanism of telomere length shortening in HCV-associated disease is largely unknown. In the present study, protein interactions between NS5A and TEN1 were confirmed by immunoprecipitation assays. Silencing of TEN1 reduced both viral RNA and protein expression levels of HCV, while ectopic expression of the siRNA-resistant TEN1 recovered the viral protein level, suggesting that TEN1 was specifically required for HCV propagation. Importantly, we found that TEN1 is re-localized from the nucleus to the cytoplasm in HCV-infected cells. These data suggest that HCV exploits TEN1 to promote viral propagation and that telomere protection is compromised in HCV-infected cells. Overall, our findings provide mechanistic insight into the telomere shortening in HCV-infected cells.

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