Evidence map›Paper›PMID 9528790›Full record

ArticleMolecular and cellular biology1998

Characterization of BCE-1, a transcriptional enhancer regulated by prolactin and extracellular matrix and modulated by the state of histone acetylation.

C A Myers, C Schmidhauser, J Mellentin-Michelotti, G Fragoso, C D Roskelley, G Casperson, R Mossi, P Pujuguet, G Hager, M J Bissell

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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 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
6.8field-weighted citation impact, top 3% 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

45 citing papers in PubMed, 103 citations in OpenAlex.

  1. Article
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  7. Growth of lung cancer cells in three-dimensional microenvironments reveals key features of tumor malignancy.Integrative biology : quantitative biosciences from nano to macro · 2012
    Article
  8. Article
  9. Article
  10. Article
  11. The contribution of adhesion signaling to lactogenesis.Journal of cell communication and signaling · 2010
    Article
  12. Article
  13. Review
  14. Gene expression in the third dimension: the ECM-nucleus connection.Journal of mammary gland biology and neoplasia · 2010
    Review
  15. Review
  16. Review
  17. Article
  18. Article
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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

10 authors at 5 institutions in 2 countries.

C A MyersLife Sciences Division, Berkeley National Laboratory, California 94720, USA.
C Schmidhauser
J Mellentin-Michelotti
G Fragoso
C D Roskelley
G Casperson
R Mossi
P Pujuguet
G Hager
M J Bissell
Lawrence Berkeley National Laboratory · USNational Institutes of Health · USMonsanto (United States) · USNational Cancer Institute · USUniversity of Zurich · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We have previously described a 160-bp enhancer (BCE-1) in the bovine beta-casein gene that is activated in the presence of prolactin and extracellular matrix (ECM). Here we report the characterization of the enhancer by deletion and site-directed mutagenesis, electrophoretic mobility shift analysis, and in vivo footprinting. Two essential regions were identified by analysis of mutant constructions: one binds C/EBP-beta and the other binds MGF/STAT5 and an as-yet-unidentified binding protein. However, no qualitative or quantitative differences in the binding of these proteins were observed in electrophoretic mobility shift analysis using nuclear extracts derived from cells cultured in the presence or absence of ECM with or without prolactin, indicating that prolactin- and ECM-induced transcription was not dependent on the availability of these factors in the functional cell lines employed. An in vivo footprinting analysis of the factors bound to nuclear chromatin in the presence or absence of ECM and/or prolactin found no differences in the binding of C/EBP-beta but did not provide definitive results for the other factors. Neither ECM nor prolactin activated BCE-1 in transient transfections, suggesting that the chromosomal structure of the integrated template may be required for ECM-induced transcription. Further evidence is that treatment of cells with inhibitors of histone deacetylase was sufficient to induce transcription of integrated BCE-1 in the absence of ECM. Together, these results suggest that the ECM induces a complex interaction between the enhancer-bound transcription factors, the basal transcriptional machinery, and a chromosomally integrated template responsive to the acetylation state of the histones.

Indexed as

Enhancer Elements, GeneticGene Expression RegulationMilk ProteinsAcetylationAnimalsBase SequenceCaseinsCattleCCAAT-Enhancer-Binding ProteinsCell LineChromatinDNADNA-Binding ProteinsElectrophoresis, Polyacrylamide GelExtracellular MatrixHistone Deacetylase InhibitorsCaseinsCCAAT-Enhancer-Binding ProteinsChromatinDNADNA-Binding ProteinsHistone Deacetylase InhibitorsHistone DeacetylasesHistonesMilk ProteinsNuclear ProteinsProlactinSTAT5 Transcription FactorTrans-Activators

Identifiers

PMID9528790
PMCPMC121460
OpenAlexW2167517334

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.