X protein of hepatitis B virus modulates cytokine and growth factor related signal transduction pathways during the course of viral infections and hepatocarcinogenesis

Jingyu Diao, Robert Garces, Christopher D. Richardson

Producción científica: Contribución a una revistaArtículo de revisiónrevisión exhaustiva

148 Citas (Scopus)

Resumen

Hepatitis B virus produces chronic infections of the liver leading to cirrhosis and hepatocellular carcinoma. The X protein of hepatitis B virus (HBx) is a multifunctional protein that can interact with p53 but can also influence a variety of signal transduction pathways within the cell. In most instances this small viral protein favors cell survival and probably initiates hepatocarcinogenesis. HBx upregulates the activity of a number of transcription factors including NF-κB, AP-1, CREB, and TBP. However, the majority of HBx is localized to the cytoplasm where it interacts with and stimulates protein kinases such as protein kinase C, Janus kinase/STAT, IKK, PI-3-K, stress-activated protein kinase/Jun N-terminal kinase, and protein kinase B/Akt. This small viral protein can localize to the mitochondrion. HBx may act as an adaptor or kinase activator to influence signal transduction pathways. This review will attempt to analyze the involvement of HBx in signal transduction pathways during hepatitis B viral infections and hepatocellular carinoma development.

Idioma originalEnglish
Páginas (desde-hasta)189-205
Número de páginas17
PublicaciónCytokine and Growth Factor Reviews
Volumen12
N.º2-3
DOI
EstadoPublished - 2001
Publicado de forma externa

Nota bibliográfica

Funding Information:
The authors would like to thank members of the Richardson Lab and members from Ontario Cancer Institute and Amgen Research Institute for helpful discussions and comments during the preparation of this review. This research program is supported by an operating grant from the Canadian Institutes of Health Research, an Ontario Graduate Studentship, and the Amgen Research Institute.

ASJC Scopus Subject Areas

  • Endocrinology, Diabetes and Metabolism
  • Immunology and Allergy
  • Immunology
  • General Biochemistry,Genetics and Molecular Biology

PubMed: MeSH publication types

  • Journal Article
  • Research Support, Non-U.S. Gov't
  • Review

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