ArticleCellular & molecular immunology2021
SAMD4 family members suppress human hepatitis B virus by directly binding to the Smaug recognition region of viral RNA.
Article in Cellular & molecular immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 19 citations in OpenAlex.
- Restoration of HBV-specific CD8Signal transduction and targeted therapy · 2021Trial
- LAMB3 drives gastric cancer progression through SAMD4A-mediated degradation of PHLPP2 mRNA leading to sustained PI3K-Akt activation.British journal of cancer · 2026Article
- Aloe emodin isolated frommSphere · 2026Article
- Article
- Altered expression of MX2 and SAMD4A in PBMCs predicts early treatment responses in HBeAg-positive chronic hepatitis B patients during Peg-IFN-α therapy.Frontiers in pharmacology · 2026Article
- SAMD4A inhibits abdominal aortic aneurysm development and VSMC phenotypic transformation through targeting KDM2B.Journal of advanced research · 2026Article
- Oncogenic Role of SAMD4B in Breast Cancer Progression by Activating Wnt/β-Catenin Pathway.Biomolecules · 2025Article
- LSM12 promotes the lung squamous cell carcinoma progression through mediating alternative splicing of ARRB1.Communications biology · 2025Article
- The role of structure in regulatory RNA elements.Bioscience reports · 2024Review
- Interferon-γ-induced GBP1 is an inhibitor of human papillomavirus 18.BMC women's health · 2024Article
- Identification of Immunodominant Proteins of theVaccines · 2023Article
- RNA binding protein SAMD4: current knowledge and future perspectives.Cell & bioscience · 2023Review
- Role of epigenetic modification in interferon treatment of hepatitis B virus infection.Frontiers in immunology · 2022Review
- Interferon and interferon-stimulated genes in HBV treatment.Frontiers in immunology · 2022Review
- RNA-binding protein SAMD4A inhibits breast tumor angiogenesis by modulating the balance of angiogenesis program.Cancer science · 2021Article
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
HBV infection initiates hepatitis B and promotes liver cirrhosis and hepatocellular carcinoma. IFN-α is commonly used in hepatitis B therapy, but how it inhibits HBV is not fully understood. We screened 285 human interferon-stimulated genes (ISGs) for anti-HBV activity using a cell-based assay, which revealed several anti-HBV ISGs. Among these ISGs, SAMD4A was the strongest suppressor of HBV replication. We found the binding site of SAMD4A in HBV RNA, which was a previously unidentified Smaug recognition region (SRE) sequence conserved in HBV variants. SAMD4A binds to the SRE site in viral RNA to trigger its degradation. The SAM domain in SAMD4A is critical for RNA binding and the C-terminal domain of SAMD4A is required for SAMD4A anti-HBV function. Human SAMD4B is a homolog of human SAMD4A but is not an ISG, and the murine genome encodes SAMD4. All these SAMD4 proteins suppressed HBV replication when overexpressed in vitro and in vivo. We also showed that knocking out the Samd4 gene in hepatocytes led to a higher level of HBV replication in mice and AAV-delivered SAMD4A expression reduced the virus titer in HBV-producing transgenic mice. In addition, a database analysis revealed a negative correlation between the levels of SAMD4A/B and HBV in patients. Our data suggest that SAMD4A is an important anti-HBV ISG for use in IFN therapy of hepatitis B and that the levels of SAMD4A/B expression are related to HBV sensitivity in humans.
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