Evidence map›Paper›PMID 24059932›Full record

ArticleBMC molecular biology2013

Identification of an NF-κB p50/p65-responsive site in the human MIR155HG promoter.

Ryan C Thompson, Iosif Vardinogiannis, Thomas D Gilmore

Open access · hybridAbstract read
In one paragraph

Article in BMC molecular biology, 2013. 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
2.0field-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

31 citing papers in PubMed, 52 citations in OpenAlex.

  1. Article
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  6. Regulatory Non-coding RNAs in Atherosclerosis.Handbook of experimental pharmacology · 2022
    Review
  7. Review
  8. Article
  9. Myeloid MKL1 Disseminates Cues to Promote Cardiac Hypertrophy in Mice.Frontiers in cell and developmental biology · 2021
    Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
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  19. Review
  20. 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

3 authors at 1 institution in 1 country.

Ryan C ThompsonDepartment of Biology, Boston University, Boston, MA 02215, USA. gilmore@bu.edu.
Iosif Vardinogiannis
Thomas D Gilmore
Boston University · US

Funding

RESEARCH TRAINING IN BLOOD DISEASES AND RESOURCEST32HL007501 · NHLBI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI LERNER, ADAM, STEINBERG, MARTIN H. · 1985 to 2018
$5.4M
TRANSFORMATION OF CELLS BY THE V-REL ONCOGENER01CA047763 · NCI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI GILMORE, THOMAS DAVID · 1993 to 2009
$2.7M
TRANSFORMATION OF CELLS BY THE V-REL ONCOGENER29CA047763 · NCI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI GILMORE, THOMAS DAVID · 1988 to 1992
–
NCI NIH HHS CA047763NCI NIH HHS CA047763-21S3NHLBI NIH HHS T32 HL007501
6 · The paper itself

Abstract

backgroundMicroRNA-155 (miR-155) is the diced product of the MIR155HG gene. miR-155 regulates the expression of many immune-specific transcripts, is overexpressed in many human lymphomas, and has oncogenic activity in mouse transgenic models. MIR155HG has been proposed to be a target gene for transcription factor NF-κB largely due to the positive correlation between high nuclear NF-κB activity and increased miR-155 expression following treatment with NF-κB inducers or in subsets of hematopoietic cancers. Nevertheless, direct regulation of the human MIR155HG promoter by NF-κB has not been convincingly demonstrated previously.

resultsThis report shows that induction of NF-κB activity rapidly leads to increased levels of both primary MIR155HG mRNA and mature miR-155 transcripts. We have mapped an NF-κB-responsive element to a position approximately 178 nt upstream of the MIR155HG transcription start site. The -178 site is specifically bound by the NF-κB p50/p65 heterodimer and is required for p65-induced reporter gene activation. Moreover, the levels of miR-155 in nine human B-lymphoma cell lines generally correlate with increased nuclear NF-κB proteins.

conclusionOverall, the identification of an NF-κB-responsive site in the MIR155HG proximal promoter suggests that MIR155HG is a direct NF-κB target gene in vivo. Understanding NF-κB-mediated regulation of miR-155 could lead to improved immune cell-related diagnostic tools and targeted therapies.

Indexed as

Promoter Regions, Genetic3T3 CellsAnimalsBinding SitesCell Line, TumorChlorocebus aethiopsCOS CellsGene Expression Regulation, NeoplasticHumansLipopolysaccharidesMiceMice, TransgenicMicroRNAsNF-kappa B p50 SubunitSignal TransductionTranscription Factor RelALipopolysaccharidesMicroRNAsMIRN155 microRNA, humanNF-kappa B p50 SubunitTranscription Factor RelA

Identifiers

PMID24059932
PMCPMC3849010
OpenAlexW2137071089

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.