Evidence map›Paper›PMID 27775586›Full record

ArticleViruses2016

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

Abstract read
In one paragraph

Article in Viruses, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

11 citing papers in PubMed.

  1. Trial
  2. Review
  3. Article
  4. Talin‑1 interaction network in cellular mechanotransduction (Review).International journal of molecular medicine · 2022
    Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors.

Maarten A A van de KlundertDepartment of Blood-borne Infections, Sanquin Research, 1006 AD Amsterdam, The Netherlands.
Maartje van den BiggelaarDepartment of Plasma Proteins, Sanquin Research, 1006 AD Amsterdam, The Netherlands. m.vandenbiggelaar@sanquin.nl.
Neeltje A KootstraDepartment 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. n.a.kootstra@amc.uva.nl.
Hans L ZaaijerDepartment of Blood-borne Infections, Sanquin Research, 1006 AD Amsterdam, The Netherlands. h.l.zaaijer@amc.uva.nl.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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.

Indexed as

Host-Pathogen InteractionsProteolysisCell LineHepatitis B virusHumansTalinTrans-ActivatorsViral Regulatory and Accessory Proteinshepatitis B virus X proteinTalinTLN1 protein, humanTrans-ActivatorsViral Regulatory and Accessory ProteinsHBVHBV transcriptionHBxhepatitis B virusprotein XTLN1viral restriction

Identifiers

PMID27775586
PMCPMC5086613

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.