Evidence map›Paper›PMID 17939992›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2007

Herpes simplex virus-infected cell protein 0 blocks the silencing of viral DNA by dissociating histone deacetylases from the CoREST-REST complex.

Haidong Gu, Bernard Roizman

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 142 papers.

0numbers the graph read from it
0cells of the map it votes in
142citing papers in PubMed
10.6field-weighted citation impact, top 1% 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

142 citing papers in PubMed, 204 citations in OpenAlex.

  1. Article
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  3. Article
  4. Review
  5. Review
  6. Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. HSV-1 ICP0 Dimer Domain Adopts a Novel β-barrel Fold.bioRxiv : the preprint server for biology · 2024
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. A DeacetylaseViruses · 2022
    Article
  18. Histone modifiers at the crossroads of oncolytic and oncogenic viruses.Molecular therapy : the journal of the American Society of Gene Therapy · 2022
    Review
  19. Article
  20. Review

82 more citing papers are in PubMed but not listed here.

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

2 authors at 1 institution in 1 country.

Haidong GuMarjorie B. Kovler Viral Oncology Laboratories, University of Chicago, 910 East 58th Street, Chicago, IL 60637, USA.
Bernard Roizman
University of Chicago · US

Funding

Dissection Of The Functions Of Herpes Simplex Virus ICPOR37CA078766 · NCI · UNIVERSITY OF CHICAGO · PI ROIZMAN, BERNARD · 2003 to 2012
$4.4M
DISSECTION OF THE FUNCTIONS OF HERPES SIMPLEX VIRUS ICPOR01CA078766 · NCI · UNIVERSITY OF CHICAGO · PI ROIZMAN, BERNARD · 1998 to 2002
$1.1M
NCI NIH HHS CA 78766NCI NIH HHS R01 CA078766NCI NIH HHS R37 CA078766
6 · The paper itself

Abstract

A preeminent phenotype of the infected cell protein 0 (ICP0) of herpes simplex virus 1 (HSV-1) is that it acts as a promiscuous transactivator. In most cell lines exposed to DeltaICP0 mutant virus at low ratios of virus per cell infection, alpha genes are expressed but the transition to beta and gamma gene expression does not ensue, but can be enhanced by inhibitors of histone deacetylases (HDACs). Earlier studies have shown that ICP0 interacts with CoREST and displaces HDAC1 from the CoREST-REST-HDAC1/2 complex. HDAC1 and CoREST are then independently translocated to the cytoplasm. Here, we test the hypothesis that ICP0 blocks the silencing of HSV DNA by displacing HDAC1 from the CoREST-REST complex. Specifically, first, mapping studies led us to construct a truncated CoREST (CoREST(146-482)) that in transfected cells displaced HDAC1 from the CoREST-REST complex. Second, we constructed two viruses. In BACs encoding the entire HSV-1, we replaced the gene encoding ICP0 with AmpR to yield a DeltaICP0 mutant R8501. We also replaced ICP0 with CoREST(146-482) to yield recombinant R8502. The yield of R8502 mutant virus in Vero, HEp-2, and human embryonic lung cells exposed to 0.1 pfu of virus per cell was 100-, 10-, and 10-fold higher, respectively, than those of R8501 mutant virus. In Vero cells, the yield of R8502 was identical with that of wild-type virus. We conclude that CoREST(146-482) functionally replaced ICP0 and that, by extension, ICP0 acts to block the silencing of viral DNA by displacing HDAC1/2 from the CoREST-REST complex.

Indexed as

Gene SilencingAmino Acid SequenceAnimalsBinding SitesCell Line, TumorChlorocebus aethiopsDNA-Binding ProteinsDNA, ViralHistone DeacetylasesHumansImmediate-Early ProteinsMolecular Sequence DataMutant ProteinsMutationPeptidesSimplexvirusDNA-Binding ProteinsDNA, ViralHistone DeacetylasesImmediate-Early ProteinsMutant ProteinsPeptides

Identifiers

PMID17939992
PMCPMC2040395
OpenAlexW2041640338

What OpenQuestion holds

Textmetadata
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.