Search

Your search keyword '"Zhong, Jin"' showing total 8 results
Start Over Author "Zhong, Jin" Journal virology
8 results on '"Zhong, Jin"'

3. Identification of nucleotides in the 5’UTR and amino acids substitutions that are essential for the infectivity of 5’UTR-NS5A recombinant of hepatitis C virus genotype 1b (strain Con1)

Author

Li, Jinqian, primary, Feng, Shengjun, additional, Liu, Xi, additional, Guo, Mingzhe, additional, Chen, Mingxiao, additional, Chen, Yiyi, additional, Rong, Liang, additional, Xia, Jinyu, additional, Zhou, Yuanping, additional, Zhong, Jin, additional, and Li, Yi-Ping, additional

Published
2018
Full Text
View/download PDF

8. The N-terminal helix α0 of hepatitis C virus NS3 protein dictates the subcellular localization and stability of NS3/NS4A complex

Author

He, Ying, Weng, Leiyun, Li, Rui, Li, Li, Toyoda, Tetsuya, and Zhong, Jin

Subjects
*HEPATITIS C virus, *GENETIC mutation, *HELICASES, *VIRAL replication, *PROTEIN structure, *LIFE cycles (Biology)
Abstract

Abstract: The N-terminal amphipathic helix α0 of hepatitis C virus (HCV) NS3 protein is an essential structural determinant for the protein membrane association. Here, we performed functional analysis to probe the role of this helix α0 in the HCV life cycle. A point mutation M21P in this region that destroyed the helix formation disrupted the membrane association of NS3 protein and completely abolished HCV replication. Mechanistically the mutation did not affect either protease or helicase/NTPase activities of NS3, but significantly reduced the stability of NS3 protein. Furthermore, the membrane association and stability of NS3 protein can be restored by replacing the helix α0 with an amphipathic helix of the HCV NS5A protein. In summary, our data demonstrated that the amphipathic helix α0 of NS3 protein determines the proper membrane association of NS3, and this subcellular localization dictates the functional role of NS3 in the HCV life cycle. [Copyright &y& Elsevier]

Published
2012
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results