Evidence map›Paper›PMID 22976303›Full record

ArticleJournal of cell science2012

Single-cell analysis of Daxx and ATRX-dependent transcriptional repression.

Alyshia Newhart, Ilona U Rafalska-Metcalf, Tian Yang, Dmitri G Negorev, Susan M Janicki

Open access · bronzeAbstract read
In one paragraph

Article in Journal of cell science, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

38 citing papers in PubMed, 51 citations in OpenAlex.

  1. Article
  2. ATRX: From Chromatin Remodeling to Disease.Genesis (New York, N.Y. : 2000) · 2025
    Review
  3. Review
  4. Article
  5. Article
  6. Multiple Roles of dXNP and dADD1-International journal of molecular sciences · 2023
    Review
  7. Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. The Fate of Speckled Protein 100 (Sp100) During Herpesviruses Infection.Frontiers in cellular and infection microbiology · 2020
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

5 authors at 2 institutions in 1 country.

Alyshia NewhartMolecular and Cellular Oncogenesis Program, The Wistar Institute, 3601 Spruce Street, Philadelphia, PA 19104, USA.
Ilona U Rafalska-Metcalf
Tian Yang
Dmitri G Negorev
Susan M Janicki
The Wistar Institute · USUniversity of Pennsylvania · US

Funding

Tumor Microenvironment and MetastasisP30CA010815 · NCI · WISTAR INSTITUTE · PI Luis J Montaner · 1985 to 2026
$75.9M
Characterizing mechanisms of transcriptional activation using live cell imagingR01GM093000 · NIGMS · WISTAR INSTITUTE · PI JANICKI, SUSAN M · 2010 to 2014
$1.6M
NCI NIH HHS P30 CA010815NCI NIH HHS P30 CA10815NIGMS NIH HHS R01 GM093000NIGMS NIH HHS R01 GM 093000-02
6 · The paper itself

Abstract

Histone H3.3 is a constitutively expressed H3 variant implicated in the epigenetic inheritance of chromatin structures. Recently, the PML-nuclear body (PML-NB)/Nuclear Domain 10 (ND10) proteins, Daxx and ATRX, were found to regulate replication-independent histone H3.3 chromatin assembly at telomeres and pericentric heterochromatin. As it is not completely understood how PML-NBs/ND10s regulate transcription and resistance to viral infection, we have used a CMV-promoter-regulated inducible transgene array, at which Daxx and ATRX are enriched, to delineate the mechanisms through which they regulate transcription. When integrated into HeLa cells, which express both Daxx and ATRX, the array is refractory to activation. However, transcription can be induced when ICP0, the HSV-1 E3 ubiquitin ligase required to reverse latency, is expressed. As ATRX and Daxx are depleted from the activated array in ICP0-expressing HeLa cells, this suggests that they are required to maintain a repressed chromatin environment. As histone H3.3 is strongly recruited to the ICP0-activated array but does not co-localize with the DNA, this also suggests that chromatin assembly is blocked during activation. The conclusion that the Daxx and ATRX pathway is required for transcriptional repression and chromatin assembly at this site is further supported by the finding that an array integrated into the ATRX-negative U2OS cell line can be robustly activated and that histone H3.3 is similarly recruited and unincorporated into the chromatin. Therefore, this study has important implications for understanding gene silencing, viral latency and PML-NB/ND10 function.

Indexed as

Transcription, GeneticAdaptor Proteins, Signal TransducingCell Line, TumorChromatinCo-Repressor ProteinsCytomegalovirusDNA HelicasesHeLa CellsHistonesHumansMolecular ChaperonesNuclear ProteinsPromoter Regions, GeneticProtein Structure, TertiaryRepressor ProteinsSingle-Cell AnalysisAdaptor Proteins, Signal TransducingATRX protein, humanChromatinCo-Repressor ProteinsDAXX protein, humanDNA HelicasesHistonesMolecular ChaperonesNuclear ProteinsRepressor ProteinsX-linked Nuclear Protein

Identifiers

PMID22976303
PMCPMC3561858
OpenAlexW2113191529

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.