Hepatitis B Virus Protein X Induces Degradation of Talin-1

Maarten A. A. van de Klundert; Maartje van den Biggelaar; Neeltje A. Kootstra; Hans L. Zaaijer

doi:https://doi.org/10.3390/v8100281

Hepatitis B Virus Protein X Induces Degradation of Talin-1

Maarten A. A. van de Klundert, Maartje van den Biggelaar, Neeltje A. Kootstra, Hans L. Zaaijer

Research output: Contribution to journal › Article › Academic › peer-review

14 Citations (Scopus)

Abstract

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

Original language	English
Pages (from-to)	281
Journal	Viruses
Volume	8
Issue number	10
Early online date	2016
DOIs	https://doi.org/10.3390/v8100281
Publication status	Published - 2016

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https://doi.org/10.3390/v8100281

Cite this

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title = "Hepatitis B Virus Protein X Induces Degradation of Talin-1",

abstract = "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",

author = "{van de Klundert}, {Maarten A. A.} and {van den Biggelaar}, Maartje and Kootstra, {Neeltje A.} and Zaaijer, {Hans L.}",

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T1 - Hepatitis B Virus Protein X Induces Degradation of Talin-1

AU - van de Klundert, Maarten A. A.

AU - van den Biggelaar, Maartje

AU - Kootstra, Neeltje A.

AU - Zaaijer, Hans L.

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Y1 - 2016

N2 - 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

AB - 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

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DO - https://doi.org/10.3390/v8100281

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