Evidence map›Paper›PMID 28274199›Full record

ArticleBMC molecular biology2017

Properties of STAT1 and IRF1 enhancers and the influence of SNPs.

Mohamed Abou El Hassan, Katherine Huang, Manoja B K Eswara, Zhaodong Xu, Tao Yu, Arthur Aubry, Zuyao Ni, Izzy Livne-Bar, Monika Sangwan, Mohamad Ahmad and 1 more

Open access · hybridAbstract read
In one paragraph

Article in BMC molecular biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 1 pooled it
1.8field-weighted citation impact, top 14% 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

32 citing papers in PubMed, 1 synthesis or guideline pooled it, 44 citations in OpenAlex.

  1. Pooled it
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  15. Long noncoding RNAProceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  16. Genetic disruption of zebrafish mab21l1 reveals a conserved role in eye development and affected pathways.Developmental dynamics : an official publication of the American Association of Anatomists · 2021
    Article
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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

11 authors at 3 institutions in 2 countries.

Mohamed Abou El HassanLunenfeld Tanenbaum Research Institute, Mt Sinai Hospital, Toronto, ON, Canada.
Katherine HuangLunenfeld Tanenbaum Research Institute, Mt Sinai Hospital, Toronto, ON, Canada.
Manoja B K EswaraLunenfeld Tanenbaum Research Institute, Mt Sinai Hospital, Toronto, ON, Canada.
Zhaodong XuLunenfeld Tanenbaum Research Institute, Mt Sinai Hospital, Toronto, ON, Canada.
Tao YuLunenfeld Tanenbaum Research Institute, Mt Sinai Hospital, Toronto, ON, Canada.
Arthur AubryLunenfeld Tanenbaum Research Institute, Mt Sinai Hospital, Toronto, ON, Canada.
Zuyao NiLunenfeld Tanenbaum Research Institute, Mt Sinai Hospital, Toronto, ON, Canada.
Izzy Livne-BarLunenfeld Tanenbaum Research Institute, Mt Sinai Hospital, Toronto, ON, Canada.
Monika SangwanLunenfeld Tanenbaum Research Institute, Mt Sinai Hospital, Toronto, ON, Canada.
Mohamad AhmadLunenfeld Tanenbaum Research Institute, Mt Sinai Hospital, Toronto, ON, Canada.
Rod BremnerLunenfeld Tanenbaum Research Institute, Mt Sinai Hospital, Toronto, ON, Canada. bremner@lunenfeld.ca.
Lunenfeld-Tanenbaum Research Institute · CADalhousie University · CAUniversity of Toronto · CA

Funding

CIHR MOP 111004
6 · The paper itself

Abstract

backgroundSTAT1 and IRF1 collaborate to induce interferon-γ (IFNγ) stimulated genes (ISGs), but the extent to which they act alone or together is unclear. The effect of single nucleotide polymorphisms (SNPs) on in vivo binding is also largely unknown.

resultsWe show that IRF1 binds at proximal or distant ISG sites twice as often as STAT1, increasing to sixfold at the MHC class I locus. STAT1 almost always bound with IRF1, while most IRF1 binding events were isolated. Dual binding sites at remote or proximal enhancers distinguished ISGs that were responsive to IFNγ versus cell-specific resistant ISGs, which showed fewer and mainly single binding events. Surprisingly, inducibility in one cell type predicted ISG-responsiveness in other cells. Several dbSNPs overlapped with STAT1 and IRF1 binding motifs, and we developed methodology to rapidly assess their effects. We show that in silico prediction of SNP effects accurately reflects altered binding both in vitro and in vivo.

conclusionsThese data reveal broad cooperation between STAT1 and IRF1, explain cell type specific differences in ISG-responsiveness, and identify genetic variants that may participate in the pathogenesis of immune disorders.

Indexed as

Polymorphism, Single NucleotideEnhancer Elements, GeneticGenes, MHC Class IHeLa CellsHumansInterferon-gammaInterferon Regulatory Factor-1Minor Histocompatibility LociProtein BindingSTAT1 Transcription FactorUp-RegulationInterferon-gammaInterferon Regulatory Factor-1IRF1 protein, humanSTAT1 protein, humanSTAT1 Transcription Factor

Identifiers

PMID28274199
PMCPMC5343312
OpenAlexW2592370523

What OpenQuestion holds

Textmetadata
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.