Evidence map›Paper›PMID 25733689›Full record

ArticleMolecular and cellular biology2015

Promyelocytic Leukemia Protein Isoform II Promotes Transcription Factor Recruitment To Activate Interferon Beta and Interferon-Responsive Gene Expression.

Yixiang Chen, Jordan Wright, Xueqiong Meng, Keith N Leppard

Open access · hybridAbstract read
In one paragraph

Article in Molecular and cellular biology, 2015. 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
1.4field-weighted citation impact, top 19% 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

28 citing papers in PubMed, 48 citations in OpenAlex.

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  19. The Role of Promyelocytic Leukemia Nuclear Bodies During HPV Infection.Frontiers in cellular and infection microbiology · 2020
    Review
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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

4 authors at 1 institution in 1 country.

Yixiang ChenSchool of Life Sciences, University of Warwick, Coventry, United Kingdom.
Jordan WrightSchool of Life Sciences, University of Warwick, Coventry, United Kingdom.
Xueqiong MengSchool of Life Sciences, University of Warwick, Coventry, United Kingdom.
Keith N LeppardSchool of Life Sciences, University of Warwick, Coventry, United Kingdom Keith.Leppard@warwick.ac.uk.
University of Warwick · GB

Funding

LCenter for Clinical and Translational Science and TrainingUL1TR001425 · NCATS · UNIVERSITY OF CINCINNATI · PI HEUBI, JAMES E., KISSELA, BRETT M · 2015 to 2024
$37.5M
Cincinnati Center for Clinical and Translational Sciences and TrainingUL1TR000077 · NCATS · UNIVERSITY OF CINCINNATI · PI HEUBI, JAMES E., TSEVAT, JOEL · 2012 to 2014
$9.9M
NCATS NIH HHS UL1 TR000077NCATS NIH HHS UL1 TR001425Wellcome Trust WT094713MA
6 · The paper itself

Abstract

To trigger type I interferon (IFN) responses, pattern recognition receptors activate signaling cascades that lead to transcription of IFN and IFN-stimulated genes (ISGs). The promyelocytic leukemia (PML) protein has been implicated in these responses, although its role has not been defined. Here, we show that PML isoform II (PML-II) is specifically required for efficient induction of IFN-β transcription and of numerous ISGs, acting at the point of transcriptional complex assembly on target gene promoters. PML-II associated with specific transcription factors NF-κB and STAT1, as well as the coactivator CREB-binding protein (CBP), to facilitate transcriptional complex formation. The absence of PML-II substantially reduced binding of these factors and IFN regulatory factor 3 (IRF3) to IFN-β or ISGs promoters and sharply reduced gene activation. The unique C-terminal domain of PML-II was essential for its activity, while the N-terminal RBCC motif common to all PML isoforms was dispensable. We propose a model in which PML-II contributes to the transcription of multiple genes via the association of its C-terminal domain with relevant transcription complexes, which promotes the stable assembly of these complexes at promoters/enhancers of target genes, and that in this way PML-II plays a significant role in the development of type I IFN responses.

Indexed as

Cell LineGene Expression RegulationHEK293 CellsHeLa CellsHumansImmunity, InnateInterferon-betaInterferon Regulatory Factor-3Nuclear ProteinsPromoter Regions, GeneticPromyelocytic Leukemia ProteinProtein IsoformsSignal TransductionTranscription FactorsTumor Suppressor ProteinsInterferon-betaInterferon Regulatory Factor-3IRF3 protein, humanNuclear ProteinsPML protein, humanPromyelocytic Leukemia ProteinProtein IsoformsTranscription FactorsTumor Suppressor Proteins

Identifiers

PMID25733689
PMCPMC4405644
OpenAlexW2166517403

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.