Evidence map›Paper›PMID 22747694›Full record

ArticleGenome biology2012

E2F mediates enhanced alternative polyadenylation in proliferation.

Ran Elkon, Jarno Drost, Gijs van Haaften, Mathias Jenal, Mariette Schrier, Joachim A F Oude Vrielink, Reuven Agami

Open access · goldAbstract read
In one paragraph

Article in Genome biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 99 papers.

0numbers the graph read from it
0cells of the map it votes in
99citing papers in PubMed
5.8field-weighted citation impact, top 3% 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

99 citing papers in PubMed, 157 citations in OpenAlex.

  1. Review
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  5. Coupling of alternative splicing and alternative polyadenylation.Acta biochimica et biophysica Sinica · 2024
    Review
  6. Article
  7. Review
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  9. Downregulation of apoptotic repressorProceedings of the National Academy of Sciences of the United States of America · 2023
    Article
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  11. Review
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  15. Article
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  19. Dynamic alternative polyadenylation during iPSC differentiation into cardiomyocytes.Computational and structural biotechnology journal · 2022
    Article
  20. Article

39 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

7 authors at 2 institutions in 2 countries.

Ran Elkon
Jarno Drost
Gijs van Haaften
Mathias Jenal
Mariette Schrier
Joachim A F Oude Vrielink
Reuven Agami
The Netherlands Cancer Institute · NLOncode Institute · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe majority of mammalian genes contain multiple poly(A) sites in their 3' UTRs. Alternative cleavage and polyadenylation are emerging as an important layer of gene regulation as they generate transcript isoforms that differ in their 3' UTRs, thereby modulating genes' response to 3' UTR-mediated regulation. Enhanced cleavage at 3' UTR proximal poly(A) sites resulting in global 3' UTR shortening was recently linked to proliferation and cancer. However, mechanisms that regulate this enhanced alternative polyadenylation are unknown.

resultsHere, we explored, on a transcriptome-wide scale, alternative polyadenylation events associated with cellular proliferation and neoplastic transformation. We applied a deep-sequencing technique for identification and quantification of poly(A) sites to two human cellular models, each examined under proliferative, arrested and transformed states. In both cell systems we observed global 3' UTR shortening associated with proliferation, a link that was markedly stronger than the association with transformation. Furthermore, we found that proliferation is also associated with enhanced cleavage at intronic poly(A) sites. Last, we found that the expression level of the set of genes that encode for 3'-end processing proteins is globally elevated in proliferation, and that E2F transcription factors contribute to this regulation.

conclusionsOur results comprehensively identify alternative polyadenylation events associated with cellular proliferation and transformation, and demonstrate that the enhanced alternative polyadenylation in proliferative conditions results not only in global 3' UTR shortening but also in enhanced premature cleavage in introns. Our results also indicate that E2F-mediated co-transcriptional regulation of 3'-end processing genes is one of the mechanisms that links enhanced alternative polyadenylation to proliferation.

Indexed as

3' Untranslated RegionsCell LineCell ProliferationCell Transformation, NeoplasticE2F Transcription FactorsFibroblastsGene Expression ProfilingHigh-Throughput Nucleotide SequencingHumansPoly APolyadenylationSequence Analysis, RNA3' Untranslated RegionsE2F Transcription FactorsPoly A

Identifiers

PMID22747694
PMCPMC3491381
OpenAlexW2130907011

What OpenQuestion holds

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LicenceCC BY
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.