ArticleExperimental and therapeutic medicine2021
Role of STAT1 in the resistance of HBV to IFN-α.
Article in Experimental and therapeutic medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 7 citations in OpenAlex.
- Repurposing Product Nkabinde for Hepatitis B Virus Therapy: A Network Pharmacology and Molecular Docking Investigation.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Interferon-alpha 2b (IFNα2b) enhances monocyte-derived dendritic cell maturation and Th1-skewed anti-tumor immunity in non-small cell lung cancer.Molecular biology reports · 2025Article
- Contradictory Mechanisms of rheumatoid arthritis and hepatitis B virus infection activation.Heliyon · 2025Review
- Development and validation of biomarkers related to anoikis in liver cirrhosis based on bioinformatics analysis.World journal of hepatology · 2024Article
- Targeting mitochondrial damage: shining a new light on immunotherapy.Frontiers in immunology · 2024Review
- Role of hepatitis B virus non-structural protein HBx on HBV replication, interferon signaling, and hepatocarcinogenesis.Frontiers in microbiology · 2023Review
- IFN-Mediators of inflammation · 2023Article
Corrections and comments
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Authors and funding
3 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The objective of the present study was to explore the mechanism of hepatitis B virus (HBV) resistance to interferon (IFN), and the role of signal transducer and activator of transcription 1 (STAT1). HepG2.2.15 cells were stimulated with a long-term (6-24 weeks) low-dose interferon (IFN)α-2b (10-70 IU/ml), so as to construct and screen a HepG2.2.15 cell model resistant to IFNα-2b. The changes of STAT1 and other proteins in the JAK-STAT signaling pathway, before and after drug resistance, were compared. The phosphorylation of STAT1 in HepG2.2.15 cells resistant to IFNα-2b was significantly decreased, and the expression level of 2',5'-oligoadenylate synthetase 1 was downregulated. Decreased phosphorylation of STAT1 in the JAK-STAT signaling pathway a contributor to the development of resistance to IFN-α in HBV.
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Registered trials
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