Evidence map›Paper›PMID 27866206›Full record

ArticleJournal of innate immunity2017

Genome-Wide STAT3 Binding Analysis after Histone Deacetylase Inhibition Reveals Novel Target Genes in Dendritic Cells.

Yaping Sun, Matthew Iyer, Richard McEachin, Meng Zhao, Yi-Mi Wu, Xuhong Cao, Katherine Oravecz-Wilson, Cynthia Zajac, Nathan Mathewson, Shin-Rong Julia Wu and 5 more

Open access · goldAbstract read
In one paragraph

Article in Journal of innate immunity, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.0field-weighted citation impact, top 21% 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

8 citing papers in PubMed, 13 citations in OpenAlex.

  1. Review
  2. STAT3 SH2 Domain Aspartic Acid 661 Mutations Activate Immune Gene Programs.Journal of cellular and molecular medicine · 2026
    Article
  3. Article
  4. Article
  5. Biology and therapeutic potential of interleukin-10.The Journal of experimental medicine · 2020
    Review
  6. Review
  7. Article
  8. STAT3 Expression in Host Myeloid Cells Controls Graft-versus-Host Disease Severity.Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation · 2017
    Article
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

15 authors at 3 institutions in 1 country.

Yaping SunDivision of Hematology/Oncology, Department of Internal Medicine, University of Michigan, Ann Arbor, Mich., USA.
Matthew Iyer
Richard McEachin
Meng Zhao
Yi-Mi Wu
Xuhong Cao
Katherine Oravecz-Wilson
Cynthia Zajac
Nathan Mathewson
Shin-Rong Julia Wu
Corinne Rossi
Tomomi Toubai
Zhaohui S Qin
Arul M Chinnaiyan
Pavan Reddy
Howard Hughes Medical Institute · USEmory University · USUniversity of Michigan–Ann Arbor · US

Funding

MICHIGAN MEDICAL SCIENTIST TRAINING PROGRAMT32GM007863 · NIGMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI COLLINS, KATHLEEN L. · 1985 to 2024
$38.3M
Targeting antigen presentation to enhance GVL responses after Bone Marrow TransplR01HL090775 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI REDDY, PAVAN · 2008 to 2016
$3.4M
Cellular and molecular mechanisms of target tissue resistance for mitigating GVHD severityR01CA203542 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI REDDY, PAVAN · 2016 to 2020
$2.4M
Development of novel strategy for treatment of steroid refractory GVHDR01HL128046 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI REDDY, PAVAN · 2015 to 2019
$2.1M
Role of noncoding RNA in Regulating GVHDR01CA173878 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI REDDY, PAVAN · 2013 to 2017
$1.6M
Development of a Novel Strategy to Prevent Experimental GVHDR01CA143379 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI REDDY, PAVAN · 2010 to 2014
$739k
NCI NIH HHS R01 CA143379NCI NIH HHS R01 CA173878NCI NIH HHS R01 CA203542NHLBI NIH HHS R01 HL090775NHLBI NIH HHS R01 HL128046NIGMS NIH HHS T32 GM007863
6 · The paper itself

Abstract

STAT3 is a master transcriptional regulator that plays an important role in the induction of both immune activation and immune tolerance in dendritic cells (DCs). The transcriptional targets of STAT3 in promoting DC activation are becoming increasingly understood; however, the mechanisms underpinning its role in causing DC suppression remain largely unknown. To determine the functional gene targets of STAT3, we compared the genome-wide binding of STAT3 using ChIP sequencing coupled with gene expression microarrays to determine STAT3-dependent gene regulation in DCs after histone deacetylase (HDAC) inhibition. HDAC inhibition boosted the ability of STAT3 to bind to distinct DNA targets and regulate gene expression. Among the top 500 STAT3 binding sites, the frequency of canonical motifs was significantly higher than that of noncanonical motifs. Functional analysis revealed that after treatment with an HDAC inhibitor, the upregulated STAT3 target genes were those that were primarily the negative regulators of proinflammatory cytokines and those in the IL-10 signaling pathway. The downregulated STAT3-dependent targets were those involved in immune effector processes and antigen processing/presentation. The expression and functional relevance of these genes were validated. Specifically, functional studies confirmed that the upregulation of IL-10Ra by STAT3 contributed to the suppressive function of DCs following HDAC inhibition.

Indexed as

AnimalsAntigen PresentationBone Marrow CellsCell DifferentiationCells, CulturedDendritic CellsFemaleGene Expression RegulationGenomeHigh-Throughput Nucleotide SequencingHistone Deacetylase InhibitorsInterleukin-10MiceMice, Inbred BALB CMice, Inbred C57BLMicroarray AnalysisHistone Deacetylase InhibitorsInterleukin-10Receptors, Interleukin-10Stat3 protein, mouseSTAT3 Transcription Factor

Identifiers

PMID27866206
PMCPMC5330838
OpenAlexW2552623127

What OpenQuestion holds

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LicenceTDM
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.