Evidence map›Paper›PMID 18955504›Full record

ArticleMolecular and cellular biology2009

Chromatin immunoprecipitation on microarray analysis of Smad2/3 binding sites reveals roles of ETS1 and TFAP2A in transforming growth factor beta signaling.

Daizo Koinuma, Shuichi Tsutsumi, Naoko Kamimura, Hirokazu Taniguchi, Keiji Miyazawa, Makoto Sunamura, Takeshi Imamura, Kohei Miyazono, Hiroyuki Aburatani

Abstract read
In one paragraph

Article in Molecular and cellular biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 124 papers.

0numbers the graph read from it
0cells of the map it votes in
124citing papers in PubMed
4.8field-weighted citation impact, top 4% 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

124 citing papers in PubMed, 201 citations in OpenAlex.

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  9. Analysis of the DNA-binding properties of TGF-β-activated Smad complexes unveils a possible molecular basis for cellular context-dependent signaling.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024
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  20. Genetic polymorphisms ofFrontiers in genetics · 2022
    Article

64 more citing papers are in PubMed but not listed here.

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

9 authors at 4 institutions in 1 country.

Daizo KoinumaDepartment of Biochemistry, The Cancer Institute of the Japanese Foundation for Cancer Research, Koto-ku, Tokyo 135-8550, Japan.
Shuichi Tsutsumi
Naoko Kamimura
Hirokazu Taniguchi
Keiji Miyazawa
Makoto Sunamura
Takeshi Imamura
Kohei Miyazono
Hiroyuki Aburatani
The University of Tokyo · JPJapanese Foundation For Cancer Research · JPNational Cancer Center Hospital East · JPTohoku University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The Smad2 and Smad3 (Smad2/3) proteins are principally involved in the transmission of transforming growth factor beta (TGF-beta) signaling from the plasma membrane to the nucleus. Many transcription factors have been shown to cooperate with the Smad2/3 proteins in regulating the transcription of target genes, enabling appropriate gene expression by cells. Here we identified 1,787 Smad2/3 binding sites in the promoter regions of over 25,500 genes by chromatin immunoprecipitation on microarray in HaCaT keratinocytes. Binding elements for the v-ets erythroblastosis virus E26 oncogene homolog (ETS) and transcription factor AP-2 (TFAP2) were significantly enriched in Smad2/3 binding sites, and knockdown of either ETS1 or TFAP2A resulted in overall alteration of TGF-beta-induced transcription, suggesting general roles for ETS1 and TFAP2A in the transcription induced by TGF-beta-Smad pathways. We identified novel Smad binding sites in the CDKN1A gene where Smad2/3 binding was regulated by ETS1 and TFAP2A. Moreover, we showed that small interfering RNAs for ETS1 and TFAP2A affected TGF-beta-induced cytostasis. We also analyzed Smad2- or Smad3-specific target genes regulated by TGF-beta and found that their specificity did not appear to be solely determined by the amounts of the Smad2/3 proteins bound to the promoters. These findings reveal novel regulatory mechanisms of Smad2/3-induced transcription and provide an essential resource for understanding their roles.

Indexed as

Chromatin ImmunoprecipitationMicroarray AnalysisBinding SitesCell DeathCell LineCyclin-Dependent Kinase Inhibitor p21Gene Expression ProfilingGene Knockdown TechniquesHumansIntronsPromoter Regions, GeneticProto-Oncogene Protein c-ets-1Proto-Oncogene Proteins c-junSignal TransductionSmad2 ProteinSmad3 ProteinCDKN1A protein, humanCyclin-Dependent Kinase Inhibitor p21ETS1 protein, humanProto-Oncogene Protein c-ets-1Proto-Oncogene Proteins c-junSmad2 ProteinSMAD2 protein, humanSmad3 ProteinSMAD3 protein, humanTFAP2A protein, humanTranscription Factor AP-1Transcription Factor AP-2Transforming Growth Factor beta

Identifiers

PMID18955504
PMCPMC2612478
OpenAlexW2111391000

What Socratic 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 Socratic graph.