Evidence map›Paper›PMID 17567999›Full record

ArticleGenome research2007

Identification of an OCT4 and SRY regulatory module using integrated computational and experimental genomics approaches.

Victor X Jin, Henriette O'Geen, Sushma Iyengar, Roland Green, Peggy J Farnham

Abstract read
In one paragraph

Article in Genome research, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing 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

35 citing papers in PubMed.

  1. Article
  2. Putative contributions of the sex chromosome proteins SOX3 and SRY to neurodevelopmental disorders.American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics · 2019
    Article
  3. Article
  4. The complexity of TRIM28 contribution to cancer.Journal of biomedical science · 2017
    Review
  5. Article
  6. Article
  7. Article
  8. KAPtain in charge of multiple missions: Emerging roles of KAP1.World journal of biological chemistry · 2014
    Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. KAP1 protein: an enigmatic master regulator of the genome.The Journal of biological chemistry · 2011
    Review
  15. Functional analysis of KAP1 genomic recruitment.Molecular and cellular biology · 2011
    Article
  16. Article
  17. Transcription factor effector domains.Sub-cellular biochemistry · 2011
    Article
  18. Article
  19. Article
  20. Review
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

5 authors.

Victor X JinDepartment of Pharmacology and the Genome Center, University of California-Davis, Davis, California 95616, USA.
Henriette O'Geen
Sushma Iyengar
Roland Green
Peggy J Farnham

Funding

Discovery of Binding Sites for Transcription FactorsR01HG003129 · NHGRI · NIMBLEGEN SYSTEMS, INC. · PI GREEN, ROLAND D · 2003 to 2006
$1.6M
Mechanisms of Transcriptional Regulation in Stem CellsR01DK067889 · NIDDK · UNIVERSITY OF CALIFORNIA DAVIS · PI FARNHAM, PEGGY J · 2005 to 2007
$649k
Mechanisms of Transcriptional Regulation in Stem CellsR56DK067889 · NIDDK · UNIVERSITY OF CALIFORNIA AT DAVIS · PI FARNHAM, PEGGY J · 2009 to 2009
$222k
NCI NIH HHS CA45250NHGRI NIH HHS HG003129NHGRI NIH HHS R01 HG003129NIDDK NIH HHS DK067889NIDDK NIH HHS R01 DK067889NIDDK NIH HHS R56 DK067889
6 · The paper itself

Abstract

ChIP-chip studies have revealed that many in vivo binding sites have a weak match to the consensus sequence for the transcription factor being analyzed. Possible explanations for these observations include (1) the in vitro-derived consensus site does not represent the in vivo binding site and/or (2) the factor is recruited to a weak binding site via interaction with another protein. To address these possibilities, we developed an approach (ChIPMotifs) that incorporates a bootstrap resampling method to statistically infer the optimal cutoff threshold for a position weight matrix (PWM) of a motif identified from ChIP-chip data by ab initio motif discovery programs. Using OCT4 ChIP-chip data and the ChIPMotifs approach, we first developed a refined OCT4 PWM. We then used the refined PWM and a ChIPModules approach to identify transcription factors colocalizing with OCT4 in Ntera2 testicular embryonal carcinoma cells. We found that the consensus binding site for SRY, a transcription factor critical for testis development, colocalizes with the OCT4 PWM. To further characterize the relationship between OCT4 and SRY, we performed ChIP-chip experiments with human promoter microarrays, and found that 49% of the top approximately 1000 OCT4 target promoters were also bound by SRY. This analysis represents the first identification of SRY target promoters. Interestingly, we determined that promoters bound by OCT4 and SRY, but not those bound by SRY alone, were also bound by the transcriptional repressor KAP1. Our studies not only validate the ChIPMotifs and ChIPModules combinatorial approach but also identify a possible new regulatory partner of OCT4.

Indexed as

Response ElementsSequence Analysis, DNASoftwareComputational BiologyDNA-Binding ProteinsHumansMaleOctamer Transcription Factor-3Oligonucleotide Array Sequence AnalysisOrganogenesisRepressor ProteinsSex-Determining Region Y ProteinTestisTripartite Motif-Containing Protein 28DNA-Binding ProteinsOctamer Transcription Factor-3Repressor ProteinsSex-Determining Region Y ProteinSRY protein, humanTRIM28 protein, humanTripartite Motif-Containing Protein 28

Identifiers

PMID17567999
PMCPMC1891340

What OpenQuestion holds

Textmetadata
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Registered trials

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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.