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Updated: Jul 15, 2026

A High Resolution Method to Monitor Phosphorylation-dependent Activation of IRF3
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Published on: January 24, 2016

Cell-specific regulation of APOBEC3F by interferons.

Songcheng Ying1, Xuzhao Zhang, Phuong Thi Nguyen Sarkis

  • 1Second Affiliated Hospital, Cancer Institute, School of Medicine, Zhejiang University, Hangzhou 310009, China.

Acta Biochimica Et Biophysica Sinica
|April 10, 2007
PubMed
Summary

Human APOBEC3F (A3F) antiviral protein is upregulated by interferon-alpha in liver cells and macrophages, but not T cells. Individual variations in A3F and A3G expression may impact hepatitis B infection outcomes.

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Area of Science:

  • Immunology
  • Virology
  • Molecular Biology

Background:

  • Human cytidine deaminase APOBEC3F (A3F) exhibits broad antiviral activity against hepatitis B virus (HBV) and retroviruses like HIV-1.
  • Understanding A3F regulation in key target cells such as CD4+ T lymphocytes, macrophages, and primary liver cells is crucial but limited.

Purpose of the Study:

  • To investigate the regulation of APOBEC3F (A3F) and APOBEC3G (A3G) by interferon-alpha (IFN-alpha) in relevant human cell types.
  • To identify cell-specific differences in IFN-alpha-induced A3F expression and explore potential regulatory factors.

Main Methods:

  • Primary hepatocytes, liver cell lines, macrophages, and T lymphoid cells were treated with IFN-alpha.
  • Expression levels of A3F and A3G were analyzed, alongside the induction of other IFN-stimulated genes like PKR.

Main Results:

  • IFN-alpha upregulated A3F in primary hepatocytes, liver cell lines, and macrophages.
  • Despite active IFN-alpha signaling and induction of PKR in T lymphoid cells, A3F and A3G were not induced.
  • Significant inter-individual variability in A3F and A3G expression was observed in primary hepatocytes.

Conclusions:

  • IFN-alpha-induced A3F expression is regulated distinctly in different cell types, involving factors beyond known IFN-stimulated genes.
  • Variations in A3F and A3G expression and regulation among individuals may play a role in hepatitis B infection outcomes.