Evidence map›Paper›PMID 26776159›Full record

ArticleOncogene2016

A p53-bound enhancer region controls a long intergenic noncoding RNA required for p53 stress response.

C A Melo, N Léveillé, K Rooijers, P J Wijchers, G Geeven, A Tal, S A Melo, W de Laat, R Agami

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.0field-weighted citation impact, top 25% 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

22 citing papers in PubMed, 28 citations in OpenAlex.

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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

9 authors at 4 institutions in 2 countries.

C A MeloDivision of Biological Stress Response, The Netherlands Cancer Institute, Amsterdam, The Netherlands.
N LéveilléDivision of Biological Stress Response, The Netherlands Cancer Institute, Amsterdam, The Netherlands.
K RooijersDivision of Biological Stress Response, The Netherlands Cancer Institute, Amsterdam, The Netherlands.
P J WijchersHubrecht Institute-KNAW and University Medical Centre Utrecht, Utrecht, The Netherlands.
G GeevenHubrecht Institute-KNAW and University Medical Centre Utrecht, Utrecht, The Netherlands.
A TalDivision of Biological Stress Response, The Netherlands Cancer Institute, Amsterdam, The Netherlands.
S A MeloInstituto de Investigação e Inovação em Saúde, Universidade do Porto, Institute of Pathology and Molecular Immunology of the University of Porto (IPATIMUP), Porto, Portugal.
W de LaatHubrecht Institute-KNAW and University Medical Centre Utrecht, Utrecht, The Netherlands.
R AgamiDivision of Biological Stress Response, The Netherlands Cancer Institute, Amsterdam, The Netherlands.
The Netherlands Cancer Institute · NLHubrecht Institute for Developmental Biology and Stem Cell Research · NLErasmus MC · NLi3S - Instituto de Investigação e Inovação em Saúde, Universidade do Porto · PT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Genome-wide chromatin studies identified the tumor suppressor p53 as both a promoter and an enhancer-binding transcription factor. As an enhancer factor, p53 can induce local production of enhancer RNAs, as well as transcriptional activation of distal neighboring genes. Beyond the regulation of protein-coding genes, p53 has the capacity to regulate long intergenic noncoding RNA molecules (lincRNAs); however, their importance to the p53 tumor suppressive function remains poorly characterized. Here, we identified and characterized a novel p53-bound intronic enhancer that controls the expression of its host, the lincRNA00475 (linc-475). We demonstrate the requirement of linc-475 for the proper induction of a p53-dependent cell cycle inhibitory response. We further confirm the functional importance of linc-475 in the maintenance of CDKN1A/p21 levels, a cell cycle inhibitor and a major p53 target gene, following p53 activation. Interestingly, loss of linc-475 reduced the binding of both p53 and RNA polymerase II (RNAPII) to the promoter of p21, attenuating its transcription rate following p53 activation. Altogether, our data suggest a direct role of p53-bound enhancer domains in the activation of lincRNAs required for an efficient p53 transcriptional response.

Indexed as

Cyclin-Dependent Kinase Inhibitor p21Enhancer Elements, GeneticG1 Phase Cell Cycle CheckpointsHumansPromoter Regions, GeneticRNA, Long NoncodingRNA Polymerase IITumor Suppressor Protein p53CDKN1A protein, humanCyclin-Dependent Kinase Inhibitor p21RNA, Long NoncodingRNA Polymerase IITP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID26776159
OpenAlexW2267140735

What OpenQuestion 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 OpenQuestion graph.