Evidence map›Paper›PMID 20660350›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2010

XBP-1 couples endoplasmic reticulum stress to augmented IFN-beta induction via a cis-acting enhancer in macrophages.

Ling Zeng, Yi-Ping Liu, Haibo Sha, Hui Chen, Ling Qi, Judith A Smith

Abstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
81citing papers in PubMed, 1 pooled it
4.7field-weighted citation impact, top 5% 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

81 citing papers in PubMed, 1 synthesis or guideline pooled it, 122 citations in OpenAlex.

  1. Pooled it
  2. RNase L Regulates Antiviral Responsiveness through Cleavage of XBP1 mRNA.bioRxiv : the preprint server for biology · 2026
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  19. RIG-I Deficiency Promotes Obesity-Induced Insulin Resistance.Pharmaceuticals (Basel, Switzerland) · 2021
    Article
  20. Article

21 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

6 authors at 2 institutions in 1 country.

Ling ZengDepartment of Pediatrics, University of Wisconsin School of Medicine and Public Health, Madison, WI 53792, USA.
Yi-Ping Liu
Haibo Sha
Hui Chen
Ling Qi
Judith A Smith
Cornell University · USUniversity of Wisconsin–Madison · US

Funding

INSTITUTIONAL CTSA (UW-MADISON): CLINICAL TRIALSUL1RR025011 · NCRR · UNIVERSITY OF WISCONSIN-MADISON · PI DREZNER, MARC KENNETH · 2007 to 2011
$29.5M
Adipokine Signaling in MacrophagesR01DK082582 · NIDDK · CORNELL UNIVERSITY · PI QI, LING · 2009 to 2013
$1.6M
Regulation of IFN-beta induction by P2X7 purinergic receptor signalingK08AI081045 · NIAID · UNIVERSITY OF WISCONSIN-MADISON · PI SMITH, JUDITH ANNE · 2009 to 2011
$419k
NCRR NIH HHS KL2 UL1RR025011NCRR NIH HHS UL1 RR025011NIAID NIH HHS K08 AI081045NIAID NIH HHS KL2 K08-AI081045NIDDK NIH HHS R01 DK082582
6 · The paper itself

Abstract

Perturbation of the endoplasmic reticulum (ER) results in a conserved stress response called the unfolded protein response (UPR). Macrophages undergoing a UPR respond to LPS with log-fold increased production of IFN-beta, a cytokine with diverse roles in innate and adaptive immunity. In this study, we found that thapsigargin-induced ER stress augmented recruitment of IFN regulatory factor-3, CREB binding protein/p300, and transcriptional machinery to the murine ifnb1 promoter during LPS stimulation. Although full synergistic IFN-beta production requires X-box binding protein 1 (XBP-1), this UPR-regulated transcription factor did not appreciably bind the ifnb1 promoter. However, XBP-1 bound a conserved site 6.1 kb downstream of ifnb1, along with IFN regulatory factor-3 and CREB binding protein only during concomitant UPR and LPS stimulation. XBP-1 physically associates with p300, suggesting a mechanism of multimolecular assembly at the +6.1 kb site. Luciferase reporter assays provide evidence this +6 kb region functions as an XBP-1-dependent enhancer of ifnb1 promoter activity. Thus, this study identifies a novel role for a UPR-dependent transcription factor in the regulation of an inflammatory cytokine. Our findings have broader mechanistic implications for the pathogenesis of diseases involving ER stress and type I IFN, including viral infection, ischemia-reperfusion injury, protein misfolding, and inflammatory diseases.

Indexed as

AnimalsCell LineCells, CulturedDNA-Binding ProteinsEndoplasmic ReticulumEnhancer Elements, GeneticGene Knockout TechniquesHumansImmunoblottingInterferon-betaInterferon Regulatory Factor-3LipopolysaccharidesLuciferasesMacrophagesMiceMice, Inbred C57BLDNA-Binding ProteinsInterferon-betaInterferon Regulatory Factor-3LipopolysaccharidesLuciferasesp300-CBP Transcription FactorsRegulatory Factor X Transcription FactorsThapsigarginTranscription FactorsX-Box Binding Protein 1XBP1 protein, humanXbp1 protein, mouse

Identifiers

PMID20660350
PMCPMC2916979
OpenAlexW2105180164

What OpenQuestion holds

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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.