Evidence map›Paper›PMID 17072331›Full record

ReviewOncogene2006

Mutations in the NF-kappaB signaling pathway: implications for human disease.

G Courtois, T D Gilmore

Abstract readReview
PubMed Publisher
In one paragraph

Review in Oncogene, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 274 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
274citing papers in PubMed, 2 pooled it
14.8field-weighted citation impact, top 1% 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

274 citing papers in PubMed, 2 syntheses or guidelines pooled it, 519 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
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  17. EvaluatingMedicina (Kaunas, Lithuania) · 2024
    Article
  18. Review
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214 more citing papers are in PubMed but not listed here.

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 2 institutions in 2 countries.

G CourtoisINSERM U697, Hôpital Saint-Louis, Paris, France.
T D Gilmore
Boston University · USHôpital Saint-Louis · FR

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 CA47763
6 · The paper itself

Abstract

The nuclear factor-kappa B (NF-kappaB) signaling pathway is a multi-component pathway that regulates the expression of hundreds of genes that are involved in diverse and key cellular and organismal processes, including cell proliferation, cell survival, the cellular stress response, innate immunity and inflammation. Not surprisingly, mis-regulation of the NF-kappaB pathway, either by mutation or epigenetic mechanisms, is involved in many human and animal diseases, especially ones associated with chronic inflammation, immunodeficiency or cancer. This review describes human diseases in which mutations in the components of the core NF-kappaB signaling pathway have been implicated and discusses the molecular mechanisms by which these alterations in NF-kappaB signaling are likely to contribute to the disease pathology. These mutations can be germline or somatic and include gene amplification (e.g., REL), point mutations and deletions (REL, NFKB2, IKBA, CYLD, NEMO) and chromosomal translocations (BCL-3). In addition, human genetic diseases are briefly described wherein mutations affect protein modifiers or transducers of NF-kappaB signaling or disrupt NF-kappaB-binding sites in promoters/enhancers.

Indexed as

MutationSignal TransductionGenetic Diseases, InbornHumansNF-kappa BNF-kappa B

Identifiers

PMID17072331
OpenAlexW1966923590

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.