Evidence map›Paper›PMID 25908863›Full record

ArticleJournal of cell science2015

Inhibiting IκBβ-NFκB signaling attenuates the expression of select pro-inflammatory genes.

Sarah McKenna, Clyde J Wright

Open access · greenAbstract read
In one paragraph

Article in Journal of cell science, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.5field-weighted citation impact, top 19% 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

26 citing papers in PubMed, 36 citations in OpenAlex.

  1. Priming innate immunity and long-term outcome.Molecular and cellular pediatrics · 2026
    Review
  2. Article
  3. Effect ofInternational journal of endocrinology · 2026
    Article
  4. Article
  5. GSK3β/NF-κB -dependent transcriptional regulation of homeostatic hepatocyteAmerican journal of physiology. Gastrointestinal and liver physiology · 2024
    Article
  6. Article
  7. Article
  8. Expression of IkappaB Family in the Ovine Liver during Early Pregnancy.Animals : an open access journal from MDPI · 2023
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Circadian clock protein Rev-erbα regulates neuroinflammation.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  16. Article
  17. Consequences of early postnatal lipopolysaccharide exposure on developing lungs in mice.American journal of physiology. Lung cellular and molecular physiology · 2019
    Article
  18. Differential mMolecular cell · 2018
    Article
  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

2 authors at 1 institution in 1 country.

Sarah McKennaSection of Neonatology, Department of Pediatrics, University of Colorado School of Medicine, Aurora, CO 80045, USA sarah.mckenna@ucdenver.edu clyde.wright@ucdenver.edu.
Clyde J WrightSection of Neonatology, Department of Pediatrics, University of Colorado School of Medicine, Aurora, CO 80045, USA sarah.mckenna@ucdenver.edu clyde.wright@ucdenver.edu.
University of Colorado Denver · US

Funding

The unique role of IkBa in modulating NF-kB activity in the newborn lung.K08HL098562 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI WRIGHT, CLYDE JASON · 2010 to 2014
$670k
NHLBI NIH HHS K08 HL098562
6 · The paper itself

Abstract

Multiple mediators of septic shock are regulated by the transcription factor nuclear factor κB (NFκB). However, complete NFκB inhibition can exacerbate disease, necessitating evaluation of targeted strategies to attenuate the pro-inflammatory response. Here, we demonstrate that in murine macrophages, low-dose NFκB inhibitors specifically attenuates lipopolysaccharide (LPS)-induced IκBβ degradation and the expression of a select subset of target genes (encoding IL1β, IL6, IL12β). Gain- and loss-of-function experiments demonstrate the necessary and sufficient role of inhibitor of NFκB family member IκBβ (also known as NFKBIB) in the expression of these genes. Furthermore, both fibroblasts and macrophages isolated from IκBβ overexpressing mice demonstrate attenuated LPS-induced IκBβ-NFκB signaling and IL1β, IL6 and IL12β expression. Further confirming the role of IκBβ and its NFκB subunit binding partner cRel in LPS-induced gene expression, pre-treatment of wild-type mouse embryonic fibroblasts with a cell-permeable peptide containing the cRel nuclear localization sequence attenuated IL6 expression. We prove that LPS-induced IκBβ-NFκB signaling can be selectively modulated to attenuate the expression of select pro-inflammatory target genes, thus providing therapeutic insights for patients exposed to systemic inflammatory stress.

Indexed as

AnimalsCell LineCell NucleusFibroblastsGene ExpressionI-kappa B ProteinsInflammationInterleukinsLipopolysaccharidesMacrophagesMaleMiceMice, Inbred ICRNF-kappa BSignal TransductionI kappa B beta proteinI-kappa B ProteinsInterleukinsLipopolysaccharidesNF-kappa BInnate immune responseIκB proteinsLipopolysaccharideLPSNFκB

Identifiers

PMID25908863
PMCPMC4457027
OpenAlexW2160700592

What OpenQuestion holds

Textmetadata
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.