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Your search keyword '"Baik L. Seong"' showing total 2 results
Start Over Author "Baik L. Seong" Topic hepatitis b virus
2 results on '"Baik L. Seong"'

1. Suppression of interferon-mediated anti-HBV response by single CpG methylation in the 5'-UTR of

Author

Keo-Heun, Lim, Eun-Sook, Park, Doo Hyun, Kim, Kyung Cho, Cho, Kwang Pyo, Kim, Yong Kwang, Park, Sung Hyun, Ahn, Seung Hwa, Park, Kee-Hwan, Kim, Chang Wook, Kim, Hong Seok, Kang, Ah Ram, Lee, Soree, Park, Heewoo, Sim, Juhee, Won, Kieun, Seok, Jueng Soo, You, Jeong-Hoon, Lee, Nam-Joon, Yi, Kwang-Woong, Lee, Kyung-Suk, Suh, Baik L, Seong, and Kyun-Hwan, Kim

Subjects
Hepatitis B virus, Proteome, Down-Regulation, Methylation, Epigenesis, Genetic, Minor Histocompatibility Antigens, Repressor Proteins, Tripartite Motif Proteins, Mice, Gene Expression Regulation, Liver, Hepatocytes, Animals, Humans, CpG Islands, Interferons, 5' Untranslated Regions, Immune Evasion
Abstract

Interferons (IFNs) mediate direct antiviral activity. They play a crucial role in the early host immune response against viral infections. However, IFN therapy for HBV infection is less effective than for other viral infections.We explored the cellular targets of HBV in response to IFNs using proteome-wide screening.Using LC-MS/MS, we identified proteins downregulated and upregulated by IFN treatment in HBV X protein (HBx)-stable and control cells. We found several IFN-stimulated genes downregulated by HBx, includingWe verified our findings using a mouse model, primary human hepatocytes and human liver tissues. Our data elucidate a mechanism by which HBV evades the host innate immune system.

Published
2016

2. RPS3a Over-Expressed in HBV-Associated Hepatocellular Carcinoma Enhances the HBx-Induced NF-kB Signaling via Its Novel Chaperoning Function.

Author

Keo-Heun Lim, Kyun-Hwan Kim, Seong Il Choi, Park, Eun-Sook, Park, Seung Hwa, Kisun Ryu, Yong Kwang Park, So Young Kwon, Sung-Il Yang, Han Chu Lee, In-Kyung Sung, and Baik L. Seong

Subjects
HEPATITIS B virus, LIVER cancer, PROTEINS, AMINO acids, CELLULAR signal transduction, CARCINOGENESIS, MEDICAL statistics, RIBOSOMAL DNA
Abstract

Hepatitis B virus (HBV) infection is one of the major causes of hepatocellular carcinoma (HCC) development. Hepatitis B virus X protein (HBx) is known to play a key role in the development of hepatocellular carcinoma (HCC). Several cellular proteins have been reported to be over-expressed in HBV-associated HCC tissues, but their role in the HBV-mediated oncogenesis remains largely unknown. Here, we explored the effect of the over-expressed cellular protein, a ribosomal protein S3a (RPS3a), on the HBx-induced NF-kB signaling as a critical step for HCC development. The enhancement of HBx-induced NFkB signaling by RPS3a was investigated by its ability to translocate NF-kB (p65) into the nucleus and the knock-down analysis of RPS3a. Notably, further study revealed that the enhancement of NF-kB by RPS3a is mediated by its novel chaperoning activity toward physiological HBx. The over-expression of RPS3a significantly increased the solubility of highly aggregation-prone HBx. This chaperoning function of RPS3a for HBx is closely correlated with the enhanced NF-kB activity by RPS3a. In addition, the mutational study of RPS3a showed that its N-terminal domain (1-50 amino acids) is important for the chaperoning function and interaction with HBx. The results suggest that RPS3a, via extra-ribosomal chaperoning function for HBx, contributes to virally induced oncogenesis by enhancing HBx-induced NF-kB signaling pathway. [ABSTRACT FROM AUTHOR]

Published
2011
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