Evidence map›Paper›PMID 30986950›Full record

ReviewInternational journal of molecular sciences2019

Cellular Cullin RING Ubiquitin Ligases: Druggable Host Dependency Factors of Cytomegaloviruses.

Tanja Becker, Vu Thuy Khanh Le-Trilling, Mirko Trilling

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
4.0field-weighted citation impact, top 6% of its field
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

14 citing papers in PubMed, 35 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Deletion of the non-adjacent genesFrontiers in immunology · 2023
    Article
  5. Article
  6. Human cytomegalovirus protein RL1 degrades the antiviral factor SLFN11 via recruitment of the CRL4 E3 ubiquitin ligase complex.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. 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

3 authors at 1 institution in 1 country.

Tanja BeckerInstitute for Virology, University Hospital Essen, University Duisburg-Essen, 45147 Essen, Germany. Tanja.Becker@uk-essen.de.
Vu Thuy Khanh Le-TrillingInstitute for Virology, University Hospital Essen, University Duisburg-Essen, 45147 Essen, Germany. Khanh.Le@rlk.uk-essen.de.ORCID 0000-0002-2733-3732
Mirko TrillingInstitute for Virology, University Hospital Essen, University Duisburg-Essen, 45147 Essen, Germany. mirko.trilling@uk-essen.de.
University of Duisburg-Essen · DE

Funding

Deutsche Forschungsgemeinschaft RTG1949
6 · The paper itself

Abstract

Human cytomegalovirus (HCMV) is a ubiquitous betaherpesvirus that frequently causes morbidity and mortality in individuals with insufficient immunity, such as transplant recipients, AIDS patients, and congenitally infected newborns. Several antiviral drugs are approved to treat HCMV infections. However, resistant HCMV mutants can arise in patients receiving long-term therapy. Additionally, side effects and the risk to cause birth defects limit the use of currently approved antivirals against HCMV. Therefore, the identification of new drug targets is of clinical relevance. Recent work identified DNA-damage binding protein 1 (DDB1) and the family of the cellular cullin (Cul) RING ubiquitin (Ub) ligases (CRLs) as host-derived factors that are relevant for the replication of human and mouse cytomegaloviruses. The first-in-class CRL inhibitory compound Pevonedistat (also called MLN4924) is currently under investigation as an anti-tumor drug in several clinical trials. Cytomegaloviruses exploit CRLs to regulate the abundance of viral proteins, and to induce the proteasomal degradation of host restriction factors involved in innate and intrinsic immunity. Accordingly, pharmacological blockade of CRL activity diminishes viral replication in cell culture. In this review, we summarize the current knowledge concerning the relevance of DDB1 and CRLs during cytomegalovirus replication and discuss chances and drawbacks of CRL inhibitory drugs as potential antiviral treatment against HCMV.

Indexed as

AnimalsAntiviral AgentsCytomegalovirusHumansInterferonsProteasome Endopeptidase ComplexProtein Processing, Post-TranslationalUbiquitin-Protein LigasesAntiviral AgentsInterferonsProteasome Endopeptidase ComplexUbiquitin-Protein Ligasesantiviral drugsCullin RING ubiquitin ligasesDDB1human cytomegalovirusMLN4924

Identifiers

PMID30986950
PMCPMC6479302
OpenAlexW2926709258

What Socratic 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 Socratic graph.