Evidence map›Paper›PMID 9774645›Full record

ArticleMolecular and cellular biology1998

The immunoglobulin heavy chain locus control region increases histone acetylation along linked c-myc genes.

L Madisen, A Krumm, T R Hebbes, M Groudine

Abstract read
In one paragraph

Article in Molecular and cellular biology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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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

30 citing papers in PubMed.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Article
  6. The epigenetics of mantle cell lymphoma.Current treatment options in oncology · 2007
    Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. A major role for the TATA box in recruitment of chromatin modifying complexes to a globin gene promoter.Proceedings of the National Academy of Sciences of the United States of America · 2003
    Article
  13. Article
  14. Review
  15. Burkitt's and Burkitt-like lymphoma.Current treatment options in oncology · 2002
    Review
  16. Regulation of alternative splicing by a transcriptional enhancer through RNA pol II elongation.Proceedings of the National Academy of Sciences of the United States of America · 2002
    Article
  17. Allele-specific underacetylation of histone H4 downstream from promoters is associated with X-inactivation in human cells.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2002
    Article
  18. Transcriptional consequences of topoisomerase inhibition.Molecular and cellular biology · 2001
    Article
  19. Article
  20. 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

4 authors.

L MadisenFred Hutchinson Cancer Research Center, University of Washington School of Medicine, Seattle, Washington, USA.
A Krumm
T R Hebbes
M Groudine

Funding

C-MYC PROTO-ONCOGENE TRANSCRIPTIONAL ELONGATION BLOCKR01CA054337 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI GROUDINE, MARK T · 1991 to 2000
$550k
NCI NIH HHS CA54337
6 · The paper itself

Abstract

In chromosome translocations characteristic of Burkitt lymphomas (BL) and murine plasmacytomas, c-myc genes become juxtaposed to immunoglobulin heavy-chain (IgH) sequences, resulting in aberrant c-myc transcription. Translocated c-myc alleles that retain the first exon exhibit increased transcription from the normally minor c-myc promoter, P1, and increased transcriptional elongation through inherent pause sites proximal to the major c-myc promoter, P2. We recently demonstrated that a cassette derived from four DNase I-hypersensitive sites (HS1234) in the 3'Calpha region of the IgH locus functions as an enhancer-locus control region (LCR) and directs a similar pattern of deregulated expression of linked c-myc genes in BL and plasmacytoma cell lines. Here, we report that the HS1234 enhancer-LCR mediates a widespread increase in histone acetylation along linked c-myc genes in Raji BL cells. Significantly, the increase in acetylation was not restricted to nucleosomes within the promoter region but also was apparent upstream and downstream of the transcription start sites as well as along vector sequences. Histone hyperacetylation of control c-myc genes, which was induced by the deacetylase inhibitor trichostatin A, mimics the effect of the HS1234 enhancer on expression from the c-myc P2 promoter, but not that from the P1 promoter. These results suggest that the HS1234 enhancer stimulates transcription of c-myc by a combination of mechanisms. Whereas HS1234 activates expression from the P2 promoter through a mechanism that includes increased histone acetylation, a general increase in histone acetylation is not sufficient to explain the HS1234-mediated activation of transcription from P1.

Indexed as

AcetylationChromatinDeoxyribonuclease IEnhancer Elements, GeneticEnzyme InhibitorsGene Expression RegulationGenes, mycHistone Deacetylase InhibitorsHistonesHydroxamic AcidsImmunoglobulin Heavy ChainsNucleosomesPromoter Regions, GeneticRestriction MappingTranscription, GeneticTranslocation, GeneticChromatinDeoxyribonuclease IEnzyme InhibitorsHistone Deacetylase InhibitorsHistonesHydroxamic AcidsImmunoglobulin Heavy ChainsNucleosomestrichostatin A

Identifiers

PMID9774645
PMCPMC109215

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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.