Evidence map›Paper›PMID 18765639›Full record

ArticleMolecular and cellular biology2008

BAT3 and SET1A form a complex with CTCFL/BORIS to modulate H3K4 histone dimethylation and gene expression.

Phuongmai Nguyen, Gil Bar-Sela, Lunching Sun, Kheem S Bisht, Hengmi Cui, Elise Kohn, Andrew P Feinberg, David Gius

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

60 citing papers in PubMed, 95 citations in OpenAlex.

  1. Article
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  3. Review
  4. Review
  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. PERM1 regulates energy metabolism in the heartFrontiers in cardiovascular medicine · 2022
    Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Atractyloside mimicsInternational journal of clinical and experimental pathology · 2018
    Article
  20. BORIS: a key regulator of cancer stemness.Cancer cell international · 2018
    Review
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

8 authors at 2 institutions in 3 countries.

Phuongmai NguyenRadiation Oncology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.
Gil Bar-Sela
Lunching Sun
Kheem S Bisht
Hengmi Cui
Elise Kohn
Andrew P Feinberg
David Gius
Johns Hopkins University · USNational Institutes of Health · US

Funding

GENOMIC IMPRINTING IN CANCERR01CA065145 · NCI · JOHNS HOPKINS UNIVERSITY · PI LEVCHENKO, ANDRE · 1994 to 2011
$5.8M
MOLECULAR PATHOLOGY OF WILMS TUMOR RELATED GENES 11PR01CA054358 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI ANDREW P. FEINBERG · 1991 to 2026
$5.5M
BWS and Embryonal Tumor Suppressor Genes on 11p15R37CA054358 · NCI · JOHNS HOPKINS UNIVERSITY · PI FEINBERG, ANDREW P. · 2001 to 2009
$4.0M
Epigenetic Regulation of Gene Expression and Resistance in Tumor CellsZIABC010544 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI GIUS, DAVID · 2009 to 2010
$736k
Intramural NIH HHSNCI NIH HHS CA65145NCI NIH HHS R01 CA054358NCI NIH HHS R01 CA065145NCI NIH HHS R37 CA054358
6 · The paper itself

Abstract

Chromatin status is characterized in part by covalent posttranslational modifications of histones that regulate chromatin dynamics and direct gene expression. BORIS (brother of the regulator of imprinted sites) is an insulator DNA-binding protein that is thought to play a role in chromatin organization and gene expression. BORIS is a cancer-germ line gene; these are genes normally present in male germ cells (testis) that are also expressed in cancer cell lines as well as primary tumors. This work identifies SET1A, an H3K4 methyltransferase, and BAT3, a cochaperone recruiter, as binding partners for BORIS, and these proteins bind to the upstream promoter regions of two well-characterized procarcinogenic genes, Myc and BRCA1. RNA interference (RNAi) knockdown of BAT3, as well as SET1A, decreased Myc and BRCA1 gene expression but did not affect the binding properties of BORIS, but RNAi knockdown of BORIS prevented the assembly of BAT3 and SET1A at the Myc and BRCA1 promoters. Finally, chromatin analysis suggested that BORIS and BAT3 exert their effects on gene expression by recruiting proteins such as SET1A that are linked to changes in H3K4 dimethylation. Thus, we propose that BORIS acts as a platform upon which BAT3 and SET1A assemble and exert effects upon chromatin structure and gene expression.

Indexed as

Gene Expression Regulation, NeoplasticAnimalsBRCA1 ProteinChlorocebus aethiopsCOS CellsDNA-Binding ProteinsHCT116 CellsHistone-Lysine N-MethyltransferaseHistonesHumansLysineMethylationMolecular ChaperonesNuclear ProteinsPromoter Regions, GeneticProtein BindingASH2L protein, humanBAG6 protein, humanBRCA1 ProteinCTCFL protein, humanDNA-Binding ProteinsH19 long non-coding RNAHistone-Lysine N-MethyltransferaseHistonesLysineMolecular ChaperonesNuclear ProteinsProteinsProto-Oncogene Proteins c-mycRNA, Long NoncodingRNA, Small InterferingRNA, UntranslatedSetd1A protein, humanTranscription Factors

Identifiers

PMID18765639
PMCPMC2573239
OpenAlexW2157710443

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.