Evidence map›Paper›PMID 10022815›Full record

ArticleOncogene1999

B-MYB transactivates its own promoter through SP1-binding sites.

A Sala, B Saitta, P De Luca, M N Cervellera, I Casella, R E Lewis, R Watson, C Peschle

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

17 citing papers in PubMed, 44 citations in OpenAlex.

  1. Article
  2. Association between B-Oncology letters · 2021
    Review
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  5. Review
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  7. Review
  8. Egr-1 transactivates Bim gene expression to promote neuronal apoptosis.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011
    Article
  9. Article
  10. Article
  11. Review
  12. B-myb and C-myb play required roles in neuronal apoptosis evoked by nerve growth factor deprivation and DNA damage.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2004
    Article
  13. Article
  14. Article
  15. Article
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  17. 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

8 authors at 7 institutions in 4 countries.

A SalaDepartment of Molecular Pharmacology and Pathology, Consorzio Mario Negri Sud, S. Maria Imbaro (CH), Italy.
B Saitta
P De Luca
M N Cervellera
I Casella
R E Lewis
R Watson
C Peschle
Mario Negri Sud Foundation · ITIstituto Superiore di Sanità · ITNebraska Medical Center · USSidney Kimmel Cancer Center · USSt. Mary's Hospital · GBUniversity of Naples Federico II · ITUniversity of Pennsylvania · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

B-MYB is an ubiquitous protein required for mammalian cell growth. In this report we show that B-MYB transactivates its own promoter through a 120 bp segment proximal to the transcription start site. The B-MYB-responsive element does not contain myb-binding sites and gel-shift analysis shows that SP1, but not B-MYB, protein contained in SAOS2 cell extracts binds to the 120 bp B-myb promoter fragment. B-MYB-dependent transactivation is cooperatively increased in the presence of SP1, but not SP3 overexpression. When the SP1 elements of the B-myb promoter are transferred in front of a heterologous promoter, an increased response to B-MYB results. In contrast, c-MYB, the prototype member of the Myb family, is not able to activate the luciferase construct containing the SP1 elements. With the use of an SP1-GAL4 fusion protein, we have determined that the cooperative activation occurs through the domain A of SP1. These observations suggest that B-MYB functions as a coactivator of SP1, and that diverse combinations of myb and SP1 sites may dictate the responsiveness of myb-target genes to the various members of the myb family.

Indexed as

Cell Cycle ProteinsPromoter Regions, GeneticSaccharomyces cerevisiae ProteinsTranscriptional ActivationAdenovirus E1A ProteinsBinding SitesCell LineDNA-Binding ProteinsFungal ProteinsHerpes Simplex Virus Protein Vmw65HumansNF-kappa BOligonucleotidesProtein BindingProto-Oncogene ProteinsProto-Oncogene Proteins c-mybAdenovirus E1A ProteinsCell Cycle ProteinsDNA-Binding ProteinsFungal ProteinsGAL4 protein, S cerevisiaeHerpes Simplex Virus Protein Vmw65MYBL2 protein, humanNF-kappa BOligonucleotidesProto-Oncogene ProteinsProto-Oncogene Proteins c-mybRecombinant Fusion ProteinsSaccharomyces cerevisiae ProteinsSp1 Transcription FactorSP3 protein, humanSp3 Transcription FactorTrans-ActivatorsTranscription Factors

Identifiers

PMID10022815
OpenAlexW2322283509

What OpenQuestion holds

Texttitle and abstract
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.