Evidence map›Paper›PMID 15548137›Full record

ArticleThe Biochemical journal2005

Bromodomain analysis of Brd2-dependent transcriptional activation of cyclin A.

Anupama Sinha, Douglas V Faller, Gerald V Denis

Open access · bronzeAbstract read
In one paragraph

Article in The Biochemical journal, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed
1.5field-weighted citation impact, top 19% 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

59 citing papers in PubMed, 102 citations in OpenAlex.

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  8. BET Proteins as Attractive Targets for Cancer Therapeutics.International journal of molecular sciences · 2021
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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

3 authors at 1 institution in 1 country.

Anupama SinhaCancer Research Center, Boston University School of Medicine, 80 East Concord Street, K521, Boston, MA 02118, USA.
Douglas V Faller
Gerald V Denis
Boston University · US

Funding

XI INTERNATIONAL SYMPOSIUM ON AMYLOIDOSISP41RR010888 · NCRR · BOSTON UNIVERSITY MEDICAL CAMPUS · PI ZAIA, JOSEPH · 1996 to 2011
$18.6M
CONTROL OF CELL GROWTH BY SHORT-CHAIN FATTY ACIDSR01CA084193 · NCI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI FALLER, DOUGLAS V · 2000 to 2004
$1.4M
NOVEL, INDUCIBLE NUCLEAR KINASE LINKED TO LEUKEMIAR29CA075107 · NCI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI DENIS, GERALD V · 1997 to 2001
$242k
Biomarkers for lymphoma in a new transgenic mouse modelR03CA102889 · NCI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI DENIS, GERALD V · 2004 to 2005
$162k
NCI NIH HHS CA102889NCI NIH HHS CA75107NCI NIH HHS CA84193NCI NIH HHS R01 CA084193NCI NIH HHS R03 CA102889NCI NIH HHS R29 CA075107NCRR NIH HHS P41 RR010888
6 · The paper itself

Abstract

Cyclin A is regulated primarily through transcription control during the mammalian cell cycle. A dual mechanism of cyclin A transcriptional repression involves, on the one hand, promoter-bound inhibitory complexes of E2F transcription factors and RB (retinoblastoma) family proteins, and on the other, chromatin-directed histone deacetylase activity that is recruited to the cyclin A promoter early in the cell cycle in association with these RB proteins. This dual regulation maintains transcriptional silence of the cyclin A locus until its transcription is required in S-phase. At that time, RB family members dissociate from E2F proteins and nucleosomal restructuring of the locus takes place, to permit transcriptional activation and resultant S-phase progression to proceed. We have identified a double bromo-domain-containing protein Brd2, which exhibits apparent 'scaffold' or transcriptional adapter functions and mediates recruitment of both E2F transcription factors and chromatin-remodelling activity to the cyclin A promoter. We have shown previously that Brd2-containing nuclear, multiprotein complexes contain E2F-1 and -2. In the present study, we show that, in S-phase, they also contain histone H4-directed acetylase activity. Overexpression of Brd2 in fibroblasts accelerates the cell cycle through increased expression of cyclin A and its associated cyclin-dependent kinase activity. Chromatin immunoprecipitation studies show that Brd2 is physically present at the cyclin A promoter and its overexpression promotes increased histone H4 acetylation at the promoter as it becomes transcriptionally active, suggesting a new model for the dual regulation of cyclin A.

Indexed as

AcetyltransferasesAnimalsBromodomain Containing ProteinsCell CycleCell Cycle ProteinsCell LineCell ProliferationChromatin ImmunoprecipitationChromosomal Proteins, Non-HistoneCyclin ADNA-Binding ProteinsE2F1 Transcription FactorE2F Transcription FactorsHistone AcetyltransferasesHumansKidneyAcetyltransferasesBrd2 protein, mouseBromodomain Containing ProteinsCell Cycle ProteinsChromosomal Proteins, Non-HistoneCyclin ADNA-Binding ProteinsE2F1 protein, humanE2f1 protein, mouseE2F1 Transcription FactorE2F Transcription FactorsHistone AcetyltransferasesPhosphotransferasesProtein Serine-Threonine KinasesRetinoblastoma ProteinTranscription Factors

Identifiers

PMID15548137
PMCPMC1134954
OpenAlexW2018825057

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.