Hepatitis C virus non-structural 5A protein can enhance full-length core protein-induced nuclear factor-κ B activation

Qing Jiao Liao, Lin Bai Ye, Khalid A. Timani, Ying Long She, Xiao Jun Yang, Li Ye, Zheng Hui Wu

Research output: Contribution to journalArticle

14 Citations (Scopus)

Abstract

Aim: To study the effects of hepatitis C virus (HCV) core and non-structural 5A (NS5A) proteins on nuclear factor-κ B (NF- κ B) activity for understanding their biological function on chronic hepatitis caused by HCV infection. Methods: Luciferase assay was used to measure the activity of NF- κ B in three different cell lines cotransfected with a series of deletion mutants of core protein alone or together with NS5A protein using pNF- κ B-Luc as a reporter plasmid. Western blot and indirect immunofluorescence assays were used to confirm the expression of proteins and to detect their subcellular localization, respectively. Furthermore, Western blot was also used to detect the expression levels of NF- κ B/p65, NF- κ B/p50, and inhibitor κ B-a(I κ B-a). Results: The wild-type core protein (C191) and its mutant segments (C173 and C158) could activate NF- κ B in Huh7 cells only and activation caused by (C191) could be enhanced by NS5A protein. Moreover, the full-length core protein and its different deletion mutants alone or together with NS5A protein did not enhance the expression level of NF- κ B. The NF- κ B activity was augmented due to the dissociation of NF- κ B-I κ B complex and the degradation of I κ B-a. Conclusion: NF- κ B is the key transcription factor that can activate many genes that are involved in the cellular immune response and inflammation. Coexpression of the full-length core protein along with NS5A can enhance the NF- κ B activation, and this activation may play a significant role in chronic liver diseases including hepatocellular carcinoma associated with HCV infection.

Original languageEnglish
Pages (from-to)6433-6439
Number of pages7
JournalWorld Journal of Gastroenterology
Volume11
Issue number41
DOIs
StatePublished - 7 Nov 2005

Fingerprint

Nuclear Proteins
Hepacivirus
Proteins
Virus Diseases
Western Blotting
NFI Transcription Factors
Mutant Proteins
Chronic Hepatitis
Indirect Fluorescent Antibody Technique
Luciferases
Cellular Immunity
Liver Diseases
Hepatocellular Carcinoma
Plasmids
Chronic Disease
Transcription Factors
Inflammation
Cell Line
Genes

Keywords

  • Core protein
  • HCV
  • NF-κ B
  • NS5A

Cite this

Liao, Qing Jiao ; Ye, Lin Bai ; Timani, Khalid A. ; She, Ying Long ; Yang, Xiao Jun ; Ye, Li ; Wu, Zheng Hui. / Hepatitis C virus non-structural 5A protein can enhance full-length core protein-induced nuclear factor-κ B activation. In: World Journal of Gastroenterology. 2005 ; Vol. 11, No. 41. pp. 6433-6439.
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title = "Hepatitis C virus non-structural 5A protein can enhance full-length core protein-induced nuclear factor-κ B activation",
abstract = "Aim: To study the effects of hepatitis C virus (HCV) core and non-structural 5A (NS5A) proteins on nuclear factor-κ B (NF- κ B) activity for understanding their biological function on chronic hepatitis caused by HCV infection. Methods: Luciferase assay was used to measure the activity of NF- κ B in three different cell lines cotransfected with a series of deletion mutants of core protein alone or together with NS5A protein using pNF- κ B-Luc as a reporter plasmid. Western blot and indirect immunofluorescence assays were used to confirm the expression of proteins and to detect their subcellular localization, respectively. Furthermore, Western blot was also used to detect the expression levels of NF- κ B/p65, NF- κ B/p50, and inhibitor κ B-a(I κ B-a). Results: The wild-type core protein (C191) and its mutant segments (C173 and C158) could activate NF- κ B in Huh7 cells only and activation caused by (C191) could be enhanced by NS5A protein. Moreover, the full-length core protein and its different deletion mutants alone or together with NS5A protein did not enhance the expression level of NF- κ B. The NF- κ B activity was augmented due to the dissociation of NF- κ B-I κ B complex and the degradation of I κ B-a. Conclusion: NF- κ B is the key transcription factor that can activate many genes that are involved in the cellular immune response and inflammation. Coexpression of the full-length core protein along with NS5A can enhance the NF- κ B activation, and this activation may play a significant role in chronic liver diseases including hepatocellular carcinoma associated with HCV infection.",
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Hepatitis C virus non-structural 5A protein can enhance full-length core protein-induced nuclear factor-κ B activation. / Liao, Qing Jiao; Ye, Lin Bai; Timani, Khalid A.; She, Ying Long; Yang, Xiao Jun; Ye, Li; Wu, Zheng Hui.

In: World Journal of Gastroenterology, Vol. 11, No. 41, 07.11.2005, p. 6433-6439.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Hepatitis C virus non-structural 5A protein can enhance full-length core protein-induced nuclear factor-κ B activation

AU - Liao, Qing Jiao

AU - Ye, Lin Bai

AU - Timani, Khalid A.

AU - She, Ying Long

AU - Yang, Xiao Jun

AU - Ye, Li

AU - Wu, Zheng Hui

PY - 2005/11/7

Y1 - 2005/11/7

N2 - Aim: To study the effects of hepatitis C virus (HCV) core and non-structural 5A (NS5A) proteins on nuclear factor-κ B (NF- κ B) activity for understanding their biological function on chronic hepatitis caused by HCV infection. Methods: Luciferase assay was used to measure the activity of NF- κ B in three different cell lines cotransfected with a series of deletion mutants of core protein alone or together with NS5A protein using pNF- κ B-Luc as a reporter plasmid. Western blot and indirect immunofluorescence assays were used to confirm the expression of proteins and to detect their subcellular localization, respectively. Furthermore, Western blot was also used to detect the expression levels of NF- κ B/p65, NF- κ B/p50, and inhibitor κ B-a(I κ B-a). Results: The wild-type core protein (C191) and its mutant segments (C173 and C158) could activate NF- κ B in Huh7 cells only and activation caused by (C191) could be enhanced by NS5A protein. Moreover, the full-length core protein and its different deletion mutants alone or together with NS5A protein did not enhance the expression level of NF- κ B. The NF- κ B activity was augmented due to the dissociation of NF- κ B-I κ B complex and the degradation of I κ B-a. Conclusion: NF- κ B is the key transcription factor that can activate many genes that are involved in the cellular immune response and inflammation. Coexpression of the full-length core protein along with NS5A can enhance the NF- κ B activation, and this activation may play a significant role in chronic liver diseases including hepatocellular carcinoma associated with HCV infection.

AB - Aim: To study the effects of hepatitis C virus (HCV) core and non-structural 5A (NS5A) proteins on nuclear factor-κ B (NF- κ B) activity for understanding their biological function on chronic hepatitis caused by HCV infection. Methods: Luciferase assay was used to measure the activity of NF- κ B in three different cell lines cotransfected with a series of deletion mutants of core protein alone or together with NS5A protein using pNF- κ B-Luc as a reporter plasmid. Western blot and indirect immunofluorescence assays were used to confirm the expression of proteins and to detect their subcellular localization, respectively. Furthermore, Western blot was also used to detect the expression levels of NF- κ B/p65, NF- κ B/p50, and inhibitor κ B-a(I κ B-a). Results: The wild-type core protein (C191) and its mutant segments (C173 and C158) could activate NF- κ B in Huh7 cells only and activation caused by (C191) could be enhanced by NS5A protein. Moreover, the full-length core protein and its different deletion mutants alone or together with NS5A protein did not enhance the expression level of NF- κ B. The NF- κ B activity was augmented due to the dissociation of NF- κ B-I κ B complex and the degradation of I κ B-a. Conclusion: NF- κ B is the key transcription factor that can activate many genes that are involved in the cellular immune response and inflammation. Coexpression of the full-length core protein along with NS5A can enhance the NF- κ B activation, and this activation may play a significant role in chronic liver diseases including hepatocellular carcinoma associated with HCV infection.

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