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Viruses 2016, 8(10), 281;

Hepatitis B Virus Protein X Induces Degradation of Talin-1

Department of Blood-borne Infections, Sanquin Research, 1006 AD Amsterdam, The Netherlands
Department of Experimental Immunology, Landsteiner Laboratory, and Center for Infectious Diseases and Immunity Amsterdam (CINIMA), Academic Medical Center of the University of Amsterdam, 1105 AZ Amsterdam, The Netherlands
Department of Plasma Proteins, Sanquin Research, 1006 AD Amsterdam, The Netherlands
These authors contributed equally to this work.
Author to whom correspondence should be addressed.
Academic Editor: Andrew Mehle
Received: 7 July 2016 / Revised: 6 October 2016 / Accepted: 9 October 2016 / Published: 19 October 2016
(This article belongs to the Section Animal Viruses)
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In the infected human hepatocyte, expression of the hepatitis B virus (HBV) accessory protein X (HBx) is essential to maintain viral replication in vivo. HBx critically interacts with the host damaged DNA binding protein 1 (DDB1) and the associated ubiquitin ligase machinery, suggesting that HBx functions by inducing the degradation of host proteins. To identify such host proteins, we systematically analyzed the HBx interactome. One HBx interacting protein, talin-1 (TLN1), was proteasomally degraded upon HBx expression. Further analysis showed that TLN1 levels indeed modulate HBV transcriptional activity in an HBx-dependent manner. This indicates that HBx-mediated TLN1 degradation is essential and sufficient to stimulate HBV replication. Our data show that TLN1 can act as a viral restriction factor that suppresses HBV replication, and suggest that the HBx relieves this restriction by inducing TLN1 degradation. View Full-Text
Keywords: hepatitis B virus; protein X; TLN1; HBx; HBV; viral restriction; HBV transcription hepatitis B virus; protein X; TLN1; HBx; HBV; viral restriction; HBV transcription

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van de Klundert, M.A.A.; van den Biggelaar, M.; Kootstra, N.A.; Zaaijer, H.L. Hepatitis B Virus Protein X Induces Degradation of Talin-1. Viruses 2016, 8, 281.

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