The transcriptional function of the hepatitis B virus X protein and its role in hepatocarcinogenesis (Review).
The hepatitis B virus (HBV) encodes a 16.5 kDa multifunctional protein termed pX or HBx, required for transcription of the viral genome and implicated in the development of hepatocellular carcinoma (HCC) in chronic HBV-infected patients. However, the mechanism of pX-mediated hepatocarcinogenesis remains unknown. pX is a multifunctional protein exhibiting a number of activities affecting transcription, cell growth, and apoptotic cell death. Although pX does not directly bind DNA, pX is regarded as a promiscuous transactivator, acting via a dual mechanism: in the cytoplasm, pX activates mitogenic signaling cascades; in the nucleus, pX interacts directly with members of the bZip class of transcription factors and with specific components of the basal transcriptional apparatus. The focus of this review is to describe the transactivation function of pX and its role in hepatocarcinogenesis.
No Reference information available - sign in for access.
No Citation information available - sign in for access.
No Supplementary Data.
No Article Media
Document Type: Research Article
Affiliations: Department of Basic Medical Sciences, Purdue University, West Lafayette, IN 47907-1246, USA.
Publication date: January 1, 1999
More about this publication?
- The International Journal of Oncology provides an international forum for the publication of the latest, cutting-edge research in the broad area of oncology and cancer treatment. The journal accepts original high quality works and reviews on all aspects of oncology research including carcinogenesis, metastasis, epidemiology, chemotherapy and viral oncology. Through fair and efficient peer review, the journal is dedicated to publishing top tier research in the field, offering authors rapid publication as well as high standards of copy-editing and production. The International Journal of Oncology is published on a monthly basis in both print and early online.
- Editorial Board
- Information for Authors
- Submit a Paper
- Subscribe to this Title
- Information for Advertisers
- Terms & Conditions
- Ingenta Connect is not responsible for the content or availability of external websites