Next Article in Journal
Human Umbilical Cord Blood Stem Cells: Rational for Use as a Neuroprotectant in Ischemic Brain Disease
Previous Article in Journal
The Chemical Master Equation Approach to Nonequilibrium Steady-State of Open Biochemical Systems: Linear Single-Molecule Enzyme Kinetics and Nonlinear Biochemical Reaction Networks
Article Menu

Export Article

Open AccessArticle
Int. J. Mol. Sci. 2010, 11(9), 3501-3512; doi:10.3390/ijms11093501

Interferon-alpha Induces High Expression of APOBEC3G and STAT-1 in Vitro and in Vivo

Department of Infectious Diseases, Renmin Hospital of Wuhan University, Wuhan 430060, China
Author to whom correspondence should be addressed.
Received: 23 August 2010 / Revised: 13 September 2010 / Accepted: 14 September 2010 / Published: 20 September 2010
(This article belongs to the Section Biochemistry, Molecular and Cellular Biology)
View Full-Text   |   Download PDF [354 KB, uploaded 19 June 2014]   |  


To investigate whether the JAK-STAT (Janus kinase-signal transducers and activators of transcription) pathway participates in the regulation of APOBEC3G (Apolipoprotein B mRNA-editing enzyme, catalytic polypeptide-like 3G) gene transcription and to study the molecular mechanisms of interferon resistance in patients with chronic hepatitis B (CHB), changes in APOBEC3G and STAT-1 expression levels in HepG2.2.15 cells after treatment with various concentrations of IFN-a, were detected using real-time RT-PCR and Western-blot. In addition, the differences in STAT-1 and APOBEC3G expression in liver tissues were also observed in patients with different anti-viral responses to IFN-a. It is found that IFN-a suppressed HBV replication and expression markedly in HepG2.2.15 cells, and simultaneously enhanced APOBEC3G expression in a dose- or time-dependent manner within a certain range. Moreover, a corresponding gradual increase in STAT-1 expression levels was also observed. The expression levels of STAT-1 and APOBEC3G in the liver of CHB patients with a complete response to IFN-a are significantly higher than that of the patients with non-response to IFN-a treatment. It is suggested that inducing intracellular APOBEC3G expression may be one of anti-HBV mechanisms of IFN-a, and IFN-a-induced APOBEC3G expression may be via the JAK-STAT signaling pathway. Moreover, interferon resistance may be related to the down-regulation of STAT-1 expression in the patients who had non-response to IFN-a treatment. View Full-Text
Keywords: STAT-1; interferon-alpha; APOBEC3G; HepG2.2.15 cell; chronic hepatitis B STAT-1; interferon-alpha; APOBEC3G; HepG2.2.15 cell; chronic hepatitis B

This is an open access article distributed under the Creative Commons Attribution License (CC BY 3.0).

Scifeed alert for new publications

Never miss any articles matching your research from any publisher
  • Get alerts for new papers matching your research
  • Find out the new papers from selected authors
  • Updated daily for 49'000+ journals and 6000+ publishers
  • Define your Scifeed now

SciFeed Share & Cite This Article

MDPI and ACS Style

Chen, H.; Wang, L.-W.; Huang, Y.-Q.; Gong, Z.-J. Interferon-alpha Induces High Expression of APOBEC3G and STAT-1 in Vitro and in Vivo. Int. J. Mol. Sci. 2010, 11, 3501-3512.

Show more citation formats Show less citations formats

Related Articles

Article Metrics

Article Access Statistics



[Return to top]
Int. J. Mol. Sci. EISSN 1422-0067 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
Back to Top