Evidence map›Paper›PMID 9012818›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America1997

Activation of human B-MYB by cyclins.

A Sala, M Kundu, I Casella, A Engelhard, B Calabretta, L Grasso, M G Paggi, A Giordano, R J Watson, K Khalili and 1 more

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
7.5field-weighted citation impact, top 2% 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

49 citing papers in PubMed, 103 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. An intrinsic S/GScience (New York, N.Y.) · 2018
    Article
  9. Article
  10. Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  11. Review
  12. Article
  13. Review
  14. Aberrant expression of cyclin D1 in cancer.Signal transduction insights · 2015
    Article
  15. Article
  16. B-myb is a gene implicated in cell cycle and proliferation of breast cancer.International journal of clinical and experimental pathology · 2014
    Article
  17. Review
  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

11 authors at 3 institutions in 3 countries.

A SalaThomas Jefferson University, Kimmel Cancer Institute, Department of Microbiology-Immunology, Philadelphia, PA, USA. A_Sala@lac.jci.tju.edu
M Kundu
I Casella
A Engelhard
B Calabretta
L Grasso
M G Paggi
A Giordano
R J Watson
K Khalili
C Peschle
Istituto Superiore di Sanità · ITLudwig Cancer Research · GBJefferson Institute · US

Funding

pRb2/p130: from the mechanisms to gene therapyR01CA060999 · NCI · THOMAS JEFFERSON UNIVERSITY · PI GIORDANO, ANTONIO · 1994 to 2008
$2.6M
NCI NIH HHS R01 CA060999NCI NIH HHS R01 CA60999
6 · The paper itself

Abstract

B-MYB expression is associated with cell proliferation and recent studies have suggested that it promotes the S phase of mammalian cells. Based on its homology to the transcription factors c-MYB and A-MYB, B-MYB is thought to be involved in transcriptional regulation; however, its activity is not detectable in several cell lines. It was postulated that B-MYB function may depend on the presence of a cofactor, and recent studies suggested that B-MYB is phosphorylated specifically during S phase in murine fibroblasts. In this report we provide evidence that the product of the human B-myb gene can be activated in vivo by coexpression with cyclin A or cyclin E. Transfection studies showed that B-MYB was a weak transcriptional activator in SAOS-2 cells and was unable to promote their proliferation. In contrast, overexpression of both B-MYB and cyclin A or cyclin E caused a drastic increase in the number of SAOS-2 cells in S phase. Also, overexpression of cyclin A and cyclin E in SAOS-2 cells enhanced the ability of B-MYB, but not c-MYB, to transactivate various promoters, including the cdc2 promoter, the HIV-1-LTR, and the simian virus 40 minimal promoter. A direct role for cyclin-dependent activation of B-MYB was demonstrated using an in vitro transcription assay. These observations suggest that one mechanism by which cyclin A and E may promote the S phase is through modification and activation of B-MYB.

Indexed as

Cell Cycle ProteinsCyclin BTrans-ActivatorsCell CycleCell DivisionCell LineCyclin B1CyclinsDNA-Binding ProteinsGene Expression RegulationHumansPhosphorylationTranscriptional ActivationTranscription FactorsCCNB1 protein, humanCell Cycle ProteinsCyclin BCyclin B1CyclinsDNA-Binding ProteinsMYBL2 protein, humanTrans-ActivatorsTranscription Factors

Identifiers

PMID9012818
PMCPMC19547
OpenAlexW2066051125

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.