1. Academic Validation
  2. Abl Tyrosine Kinase Regulates Hepatitis C Virus Entry

Abl Tyrosine Kinase Regulates Hepatitis C Virus Entry

  • Front Microbiol. 2017 Jun 19;8:1129. doi: 10.3389/fmicb.2017.01129.
Saehong Min 1 2 Yun-Sook Lim 2 Dongjo Shin 1 3 Chorong Park 1 2 Jae-Bong Park 4 Seungtaek Kim 5 Marc P Windisch 3 Soon B Hwang 1 2
Affiliations

Affiliations

  • 1 Department of Biomedical Gerontology, Graduate School of Hallym UniversityChuncheon, South Korea.
  • 2 National Research Laboratory of Hepatitis C Virus and Ilsong Institute of Life Science, Hallym UniversityAnyang, South Korea.
  • 3 Hepatitis Research Laboratory, Institut Pasteur KoreaSeongnam, South Korea.
  • 4 Department of Biochemistry, College of Medicine, Hallym UniversityChuncheon, South Korea.
  • 5 Institute of Gastroenterology, Yonsei University College of MedicineSeoul, South Korea.
Abstract

Abl is a central regulator of multiple cellular processes controlling actin dynamics, proliferation, and differentiation. Here, we showed that knockdown of Abl impaired hepatitis C virus (HCV) propagation. Treatment of Abl tyrosine kinase-specific inhibitor, imatinib and dasatinib, also significantly decreased HCV RNA and protein levels in HCV-infected cells. We showed that both imatinib and dasatinib selectively inhibited HCV Infection at the entry step of HCV life cycle, suggesting that Abl kinase activity may be necessary for HCV entry. Using HCV pseudoparticle Infection assays, we verified that Abl is required for viral entry. By employing transferrin uptake and immunofluorescence assays, we further demonstrated that Abl was involved in HCV entry at a clathrin-mediated endocytosis step. These data suggest that Abl may represent a novel host factor for HCV entry.

Keywords

Abl tyrosine kinase; HCV entry; hepatitis C virus; host factor; tyrosine kinase- inhibitor; viral propagation.

Figures
Products
  • Cat. No.
    Product Name
    Description
    Target
    Research Area
  • HY-15005
    99.97%, HCV 抑制剂
    HCV