Evidence map›Paper›PMID 19736212›Full record

ArticleNucleic acids research2009

CpG-depleted promoters harbor tissue-specific transcription factor binding signals--implications for motif overrepresentation analyses.

Helge G Roider, Boris Lenhard, Aditi Kanhere, Stefan A Haas, Martin Vingron

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In one paragraph

Article in Nucleic acids research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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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

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3 · Its place in the literature

Who cites it

28 citing papers in PubMed.

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  7. Enhancer-gene specificity in development and disease.Development (Cambridge, England) · 2022
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4 · The record

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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.

Helge G RoiderMax Planck Institute for Molecular Genetics, Ihnestrasse 73, 14195 Berlin. roider@molgen.mpg.de
Boris Lenhard
Aditi Kanhere
Stefan A Haas
Martin Vingron

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Motif overrepresentation analysis of proximal promoters is a common approach to characterize the regulatory properties of co-expressed sets of genes. Here we show that these approaches perform well on mammalian CpG-depleted promoter sets that regulate expression in terminally differentiated tissues such as liver and heart. In contrast, CpG-rich promoters show very little overrepresentation signal, even when associated with genes that display highly constrained spatiotemporal expression. For instance, while approximately 50% of heart specific genes possess CpG-rich promoters we find that the frequently observed enrichment of MEF2-binding sites upstream of heart-specific genes is solely due to contributions from CpG-depleted promoters. Similar results are obtained for all sets of tissue-specific genes indicating that CpG-rich and CpG-depleted promoters differ fundamentally in their distribution of regulatory inputs around the transcription start site. In order not to dilute the respective transcription factor binding signals, the two promoter types should thus be treated as separate sets in any motif overrepresentation analysis.

Indexed as

Promoter Regions, GeneticBinding SitesCpG IslandsTranscription FactorsTranscription Factors

Identifiers

PMID19736212
PMCPMC2770660

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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.