Evidence map›Paper›PMID 18718859›Full record

ReviewGene2008

Alternative splicing in the NF-kappaB signaling pathway.

Joshua R Leeman, Thomas D Gilmore

Open access · greenAbstract readReview
In one paragraph

Review in Gene, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
1.8field-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

39 citing papers in PubMed, 67 citations in OpenAlex.

  1. Proteomic analysis of dental pulp from deciduous teeth in comparison to permanent teeth: an in-vitro study.European archives of paediatric dentistry : official journal of the European Academy of Paediatric Dentistry · 2025
    Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Impacts and mechanisms of alternative mRNA splicing in cancer metabolism, immune response, and therapeutics.Molecular therapy : the journal of the American Society of Gene Therapy · 2022
    Review
  8. The Multifaceted Roles of USP15 in Signal Transduction.International journal of molecular sciences · 2021
    Review
  9. Article
  10. Computational Methods for Predicting Functions at the mRNA Isoform Level.International journal of molecular sciences · 2020
    Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Steroid treatment can inhibit nuclear localization of members of the NF-κB pathway in human disc cells stimulated with TNF-α.European journal of orthopaedic surgery & traumatology : orthopedie traumatologie · 2015
    Article
  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.

Joshua R LeemanDepartment of Biology, Boston University, 5 Cummington Street, Boston, MA 02215, USA.
Thomas D Gilmore
Boston University · US

Funding

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 CA47763NCI NIH HHS R01 CA047763
6 · The paper itself

Abstract

Activation of transcription factor NF-kappaB can affect the expression of several hundred genes, many of which are involved in inflammation and immunity. The proper NF-kappaB transcriptional response is primarily regulated by post-translational modification of NF-kappaB signaling constituents. Herein, we review the accumulating evidence suggesting that alternative splicing of NF-kappaB signaling components is another means of controlling NF-kappaB signaling. Several alternative splicing events in both the tumor necrosis factor and Toll/interleukin-1 NF-kappaB signaling pathways can inhibit the NF-kappaB response, whereas others enhance NF-kappaB signaling. Alternative splicing of mRNAs encoding some NF-kappaB signaling components can be induced by prolonged exposure to an NF-kappaB-activating signal, such as lipopolysaccharide, suggesting a mechanism for negative feedback to dampen excessive NF-kappaB signaling. Moreover, some NF-kappaB alternative splicing events appear to be specific for certain diseases, and could serve as therapeutic targets or biomarkers.

Indexed as

Signal TransductionAlternative SplicingAnimalsHumansI-kappa B KinaseNF-kappa BToll-Like ReceptorsTumor Necrosis Factor-alphaI-kappa B KinaseNF-kappa BToll-Like ReceptorsTumor Necrosis Factor-alpha

Identifiers

PMID18718859
PMCPMC2624576
OpenAlexW1966946883

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.