Evidence map›Paper›PMID 19615063›Full record

ArticleBMC systems biology2009

An integrative ChIP-chip and gene expression profiling to model SMAD regulatory modules.

Huaxia Qin, Michael W Y Chan, Sandya Liyanarachchi, Curtis Balch, Dustin Potter, Irene J Souriraj, Alfred S L Cheng, Francisco J Agosto-Perez, Elena V Nikonova, Pearlly S Yan and 6 more

Abstract read
In one paragraph

Article in BMC systems biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
–field-weighted citation impact
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

41 citing papers in PubMed.

  1. Article
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  15. Transcriptional Control by the SMADs.Cold Spring Harbor perspectives in biology · 2016
    Review
  16. Review
  17. Article
  18. Review
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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

16 authors.

Huaxia QinHuman Cancer Genetics Program, Department of Molecular Virology, Immunology, and Medical Genetics, The Ohio State University, Columbus, OH 43210, USA. huaxia.qin@gmail.com
Michael W Y Chan
Sandya Liyanarachchi
Curtis Balch
Dustin Potter
Irene J Souriraj
Alfred S L Cheng
Francisco J Agosto-Perez
Elena V Nikonova
Pearlly S Yan
Huey-Jen Lin
Kenneth P Nephew
Joel H Saltz
Louise C Showe
Tim H M Huang
Ramana V Davuluri

Funding

Tumor Microenvironment and MetastasisP30CA010815 · NCI · WISTAR INSTITUTE · PI Luis J Montaner · 1985 to 2026
$75.9M
Predicting Drug Resistance in Cancer Genomes by DMA Methylation ProfilingU54CA113001 · NCI · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI HUANG, TIM H.-M. · 2004 to 2014
$16.1M
NCI NIH HHS P30 CA010815NCI NIH HHS U54 CA113001
6 · The paper itself

Abstract

backgroundThe TGF-beta/SMAD pathway is part of a broader signaling network in which crosstalk between pathways occurs. While the molecular mechanisms of TGF-beta/SMAD signaling pathway have been studied in detail, the global networks downstream of SMAD remain largely unknown. The regulatory effect of SMAD complex likely depends on transcriptional modules, in which the SMAD binding elements and partner transcription factor binding sites (SMAD modules) are present in specific context.

resultsTo address this question and develop a computational model for SMAD modules, we simultaneously performed chromatin immunoprecipitation followed by microarray analysis (ChIP-chip) and mRNA expression profiling to identify TGF-beta/SMAD regulated and synchronously coexpressed gene sets in ovarian surface epithelium. Intersecting the ChIP-chip and gene expression data yielded 150 direct targets, of which 141 were grouped into 3 co-expressed gene sets (sustained up-regulated, transient up-regulated and down-regulated), based on their temporal changes in expression after TGF-beta activation. We developed a data-mining method driven by the Random Forest algorithm to model SMAD transcriptional modules in the target sequences. The predicted SMAD modules contain SMAD binding element and up to 2 of 7 other transcription factor binding sites (E2F, P53, LEF1, ELK1, COUPTF, PAX4 and DR1).

conclusionTogether, the computational results further the understanding of the interactions between SMAD and other transcription factors at specific target promoters, and provide the basis for more targeted experimental verification of the co-regulatory modules.

Indexed as

AlgorithmsAnimalsBase SequenceCell LineChromatinGene Expression ProfilingGenomeHumansImmunoprecipitationMiceModels, BiologicalOligonucleotide Array Sequence AnalysisPromoter Regions, GeneticRatsReproducibility of ResultsRNA, MessengerChromatinRNA, MessengerSmad ProteinsTransforming Growth Factor beta

Identifiers

PMID19615063
PMCPMC2724489

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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.