Adenovirus infection induces HuR relocalization to facilitate virus replication
- Department of Restorative Dentistry, Hokkaido University, Faculty of Dental Medicine, Graduate School of Dental Medicine, Sapporo (Japan)
- Department of Oral Pathology and Biology, Hokkaido University, Faculty of Dental Medicine, Graduate School of Dental Medicine, Sapporo (Japan)
- Department of Oral Diagnosis and Medicine, Hokkaido University, Faculty of Dental Medicine, Graduate School of Dental Medicine, Sapporo (Japan)
- Department of Dental Radiology, Hokkaido University, Faculty of Dental Medicine, Graduate School of Dental Medicine, Sapporo (Japan)
HuR is an RNA-binding protein of the embryonic lethal abnormal vision (ELAV) family, which binds to the AU-rich element (ARE) in the 3′-untranslated region (UTR) of certain mRNAs and is involved in the nucleo-cytoplasmic export and stabilization of ARE-mRNAs. The cytoplasmic relocalization of ARE-mRNAs with several proteins such as HuR and pp32 increases in cells transformed by the adenovirus oncogene product E4orf6. Additionally, these ARE-mRNAs were stabilized and acquired the potential to transform cells. Although, the relocalization of HuR and the stabilization of ARE-mRNAs are crucial for cell transformation, evidence regarding the relationship of HuR and ARE-mRNAs with adenovirus replication is lacking. In this report, we demonstrate that adenovirus infection induces the relocation of HuR to the cytoplasm of host cells. Analysis using the luciferase-ARE fusion gene and the tetracycline (tet)-off system revealed that the process of stabilizing ARE-mRNAs is activated in adenovirus-infected cells. Heat shock treatment or knockdown-mediated depletion of HuR reduced adenovirus production. Furthermore, expression of ARE-including viral IVa2 mRNA, decreased in HuR-depleted infected cells. These results indicate that HuR plays an important role in adenovirus replication, at least in part, by up-regulating IVa2 mRNA expression and that ARE-mRNA stabilization is required for both transformation and virus replication.
- OSTI ID:
- 23134405
- Journal Information:
- Biochemical and Biophysical Research Communications, Vol. 495, Issue 2; Other Information: Copyright (c) 2017 Elsevier Inc. All rights reserved.; Country of input: International Atomic Energy Agency (IAEA); ISSN 0006-291X
- Country of Publication:
- United States
- Language:
- English
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