Evidence map›Paper›PMID 23029193›Full record

ArticlePloS one2012

Cooperativity of stress-responsive transcription factors in core hypoxia-inducible factor binding regions.

Diego Villar, Amaya Ortiz-Barahona, Laura Gómez-Maldonado, Nuria Pescador, Fátima Sánchez-Cabo, Hubert Hackl, Benjamin A T Rodriguez, Zlatko Trajanoski, Ana Dopazo, Tim H M Huang and 2 more

Abstract read
In one paragraph

Article in PloS one, 2012. 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
–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

22 citing papers in PubMed.

  1. Article
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  8. EBF1 promotes triple-negative breast cancer progression by surveillance of the HIF1α pathway.Proceedings of the National Academy of Sciences of the United States of America · 2022
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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

12 authors.

Diego VillarDepartment of Biochemistry, Universidad Autónoma de Madrid and Instituto de Investigaciones Biomedicas Alberto Sols, Madrid, Spain. dvillar@iib.uam.es
Amaya Ortiz-Barahona
Laura Gómez-Maldonado
Nuria Pescador
Fátima Sánchez-Cabo
Hubert Hackl
Benjamin A T Rodriguez
Zlatko Trajanoski
Ana Dopazo
Tim H M Huang
Pearlly S Yan
Luis Del Peso

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The transcriptional response driven by Hypoxia-inducible factor (HIF) is central to the adaptation to oxygen restriction. Despite recent characterization of genome-wide HIF DNA binding locations and hypoxia-regulated transcripts in different cell types, the molecular bases of HIF target selection remain unresolved. Herein, we combined multi-level experimental data and computational predictions to identify sequence motifs that may contribute to HIF target selectivity. We obtained a core set of bona fide HIF binding regions by integrating multiple HIF1 DNA binding and hypoxia expression profiling datasets. This core set exhibits evolutionarily conserved binding regions and is enriched in functional responses to hypoxia. Computational prediction of enriched transcription factor binding sites identified sequence motifs corresponding to several stress-responsive transcription factors, such as activator protein 1 (AP1), cAMP response element-binding (CREB), or CCAAT-enhancer binding protein (CEBP). Experimental validations on HIF-regulated promoters suggest a functional role of the identified motifs in modulating HIF-mediated transcription. Accordingly, transcriptional targets of these factors are over-represented in a sorted list of hypoxia-regulated genes. Altogether, our results implicate cooperativity among stress-responsive transcription factors in fine-tuning the HIF transcriptional response.

Indexed as

Stress, PhysiologicalAnimalsBase SequenceBinding SitesChromatin ImmunoprecipitationDNAGene Expression ProfilingHeLa CellsHumansHypoxia-Inducible Factor 1Transcription FactorsDNAHypoxia-Inducible Factor 1Transcription Factors

Identifiers

PMID23029193
PMCPMC3454324

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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.