ArticleHepatology (Baltimore, Md.)2011
Krüppel-like factor 15 activates hepatitis B virus gene expression and replication.
Article in Hepatology (Baltimore, Md.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
23 citing papers in PubMed, 38 citations in OpenAlex.
- Review
- KLF15 Transcription Activated Tachykinin Precursor 1 to Induce Perineural Invasion in Head and Neck Squamous Cell Carcinoma.Combinatorial chemistry & high throughput screening · 2025Article
- ZNF148 inhibits HBV replication by downregulating RXRα transcription.Virology journal · 2024Article
- Specificity Proteins (SP) and Krüppel-like Factors (KLF) in Liver Physiology and Pathology.International journal of molecular sciences · 2023Review
- Krüppel-like factor 15 in liver diseases: Insights into metabolic reprogramming.Frontiers in pharmacology · 2023Review
- Pathogenicity and virulence of Hepatitis B virus.Virulence · 2022Review
- MiR-181a promotes cell proliferation and migration through targeting KLF15 in papillary thyroid cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2022Article
- The Hepatitis B Virus Interactome: A Comprehensive Overview.Frontiers in microbiology · 2021Review
- Review
- Regulation of the Hepatitis B virus replication and gene expression by the multi-functional protein TARDBP.Scientific reports · 2019Article
- Human intestinal tract serves as an alternative infection route for Middle East respiratory syndrome coronavirus.Science advances · 2017Article
- Host genes regulate transcription of sperm-introduced hepatitis B virus genes in embryo.Reproductive toxicology (Elmsford, N.Y.) · 2017Article
- A novel pyridazinone derivative inhibits hepatitis B virus replication by inducing genome-free capsid formation.Antimicrobial agents and chemotherapy · 2015Article
- Identification of TMPRSS2 as a Susceptibility Gene for Severe 2009 Pandemic A(H1N1) Influenza and A(H7N9) Influenza.The Journal of infectious diseases · 2015Article
- Inhibition of hepatitis B virus gene expression and replication by hepatocyte nuclear factor 6.Journal of virology · 2015Article
- Requirement of CRTC1 coactivator for hepatitis B virus transcription.Nucleic acids research · 2014Article
- Active replication of Middle East respiratory syndrome coronavirus and aberrant induction of inflammatory cytokines and chemokines in human macrophages: implications for pathogenesis.The Journal of infectious diseases · 2014Article
- Article
- Observational
- Diversity in genetic in vivo methods for protein-protein interaction studies: from the yeast two-hybrid system to the mammalian split-luciferase system.Microbiology and molecular biology reviews : MMBR · 2012Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
unlabelledHepatitis B virus (HBV) is a small DNA virus that requires cellular transcription factors for the expression of its genes. To understand the molecular mechanisms that regulate HBV gene expression, we conducted a yeast one-hybrid screen to identify novel cellular transcription factors that may control HBV gene expression. Here, we demonstrate that Krüppel-like factor 15 (KLF15), a liver-enriched transcription factor, can robustly activate HBV surface and core promoters. Mutations in the putative KLF15 binding site in the HBV core promoter abolished the ability of KLF15 to activate the core promoter in luciferase assays. Furthermore, the overexpression of KLF15 stimulated the expression of HBV surface antigen (HBsAg) and the core protein and enhanced viral replication. Conversely, small interfering RNA knockdown of the endogenous KLF15 in Huh7 cells resulted in a reduction in HBV surface- and core-promoter activities. In electrophoretic mobility shift and chromatin immunoprecipitation assays, KLF15 binds to DNA probes derived from the core promoter and the surface promoter. Introduction of an expression vector for KLF15 short hairpin RNA, together with the HBV genome into the mouse liver using hydrodynamic injection, resulted in a significant reduction in viral gene expression and DNA replication. Additionally, mutations in the KLF15 response element in the HBV core promoter significantly reduced viral DNA levels in the mouse serum.
conclusionKLF15 is a novel transcriptional activator for HBV core and surface promoters. It is possible that KLF15 may serve as a potential therapeutic target to reduce HBV gene expression and viral replication.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.