Evidence map›Paper›PMID 22581859›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2012

EVI1 acts as an inducible negative-feedback regulator of NF-κB by inhibiting p65 acetylation.

Xiangbin Xu, Chang-Hoon Woo, Rachel R Steere, Byung Cheol Lee, Yuxian Huang, Jing Wu, Jinjiang Pang, Jae Hyang Lim, Haidong Xu, Wenhong Zhang and 5 more

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
1.1field-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

31 citing papers in PubMed, 40 citations in OpenAlex.

  1. Article
  2. Hematology reports · 2025
    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

15 authors at 6 institutions in 5 countries.

Xiangbin XuDepartment of Microbiology and Immunology, University of Rochester Medical Center, Rochester, NY 14642, USA.
Chang-Hoon Woo
Rachel R Steere
Byung Cheol Lee
Yuxian Huang
Jing Wu
Jinjiang Pang
Jae Hyang Lim
Haidong Xu
Wenhong Zhang
Anuhya S Konduru
Chen Yan
Michael T Cheeseman
Steve D M Brown
Jian-Dong Li
University of Rochester Medical Center · USGeorgia State University · USHuashan Hospital · CNMary Lyon Centre at MRC Harwell · GBFudan University · CNInstitute of Infection and Immunity · CA

Funding

Combinational Regulation of Inflammation in Otitis MediaR01DC005843 · NIDCD · UNIVERSITY OF ROCHESTER · PI LI, JIAN-DONG · 2002 to 2016
$5.4M
UP REGULATION OF MUCIN GENE TRANSCRIPTION--OTITIS MEDIAR01DC004562 · NIDCD · UNIVERSITY OF ROCHESTER · PI LI, JIAN-DONG · 2000 to 2014
$4.7M
Regulation of Inflammation by EGFR in Otitis MediaR03DC010048 · NIDCD · UNIVERSITY OF ROCHESTER · PI XU, XIANGBIN · 2009 to 2012
$462k
Biotechnology and Biological Sciences Research Council BBS/E/D/20251969Medical Research Council MC_U142670371Medical Research Council MC_U142684172Medical Research Council MC_U142684175Medical Research Council U.1426(U.1426)NIDCD NIH HHS DC004562NIDCD NIH HHS DC005843NIDCD NIH HHS DC010048NIDCD NIH HHS R01 DC004562NIDCD NIH HHS R01 DC005843NIDCD NIH HHS R03 DC010048
6 · The paper itself

Abstract

Inflammation is a hallmark of many important human diseases. Appropriate inflammation is critical for host defense; however, an overactive response is detrimental to the host. Thus, inflammation must be tightly regulated. The molecular mechanisms underlying the tight regulation of inflammation remain largely unknown. Ecotropic viral integration site 1 (EVI1), a proto-oncogene and zinc finger transcription factor, plays important roles in normal development and leukemogenesis. However, its role in regulating NF-κB-dependent inflammation remains unknown. In this article, we show that EVI1 negatively regulates nontypeable Haemophilus influenzae- and TNF-α-induced NF-κB-dependent inflammation in vitro and in vivo. EVI1 directly binds to the NF-κB p65 subunit and inhibits its acetylation at lysine 310, thereby inhibiting its DNA-binding activity. Moreover, expression of EVI1 itself is induced by nontypeable Haemophilus influenzae and TNF-α in an NF-κB-dependent manner, thereby unveiling a novel inducible negative feedback loop to tightly control NF-κB-dependent inflammation. Thus, our study provides important insights into the novel role for EVI1 in negatively regulating NF-κB-dependent inflammation, and it may also shed light on the future development of novel anti-inflammatory strategies.

Indexed as

AcetylationAnimalsBlotting, WesternChromatin ImmunoprecipitationDNA-Binding ProteinsElectrophoretic Mobility Shift AssayFeedback, PhysiologicalHaemophilus InfectionsHaemophilus influenzaeImmunoprecipitationInflammationMDS1 and EVI1 Complex Locus ProteinMiceMice, Mutant StrainsNF-kappa BProto-Oncogene MasDNA-Binding ProteinsMAS1 protein, humanMDS1 and EVI1 Complex Locus ProteinMecom protein, mouseNF-kappa BProto-Oncogene MasRela protein, mouseTranscription Factor RelATranscription FactorsTumor Necrosis Factor-alpha

Identifiers

PMID22581859
PMCPMC3370108
OpenAlexW2134477305

What OpenQuestion holds

Textmetadata
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.