Evidence map›Paper›PMID 17666110›Full record

ReviewArthritis research & therapy2007

Falling into TRAPS--receptor misfolding in the TNF receptor 1-associated periodic fever syndrome.

Fiona C Kimberley, Adrian A Lobito, Richard M Siegel, Gavin R Screaton

Open access · goldAbstract readReview
In one paragraph

Review in Arthritis research & therapy, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 1 pooled it
1.7field-weighted citation impact, top 16% 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

32 citing papers in PubMed, 1 synthesis or guideline pooled it, 72 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Peptide-based allosteric inhibitor targets TNFR1 conformationally active region and disables receptor-ligand signaling complex.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  5. A rare missense p.C125Y mutation in theFrontiers in genetics · 2024
    Article
  6. Dermatologic Manifestations of Noninflammasome-Mediated Autoinflammatory Diseases.JID innovations : skin science from molecules to population health · 2023
    Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. Review
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  17. An expanding role for interleukin-1 blockade from gout to cancer.Molecular medicine (Cambridge, Mass.) · 2014
    Review
  18. Article
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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

4 authors at 3 institutions in 3 countries.

Fiona C KimberleyLaboratory for Experimental Oncology and Radiobiology, Academic Medical Center, Meibergdreef 9, 1105 AZ Amsterdam, The Netherlands. F.C.Kimberley@amc.uva.nl
Adrian A Lobito
Richard M Siegel
Gavin R Screaton
Academic Medical Center · NLHammersmith Hospital · GBNational Institutes of Health · US

Funding

TNF-receptors and programmed cell death in regulation of autoimmunityZIAAR041133 · NIAMS · NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES · PI SIEGEL, RICHARD M · 2009 to 2019
$9.3M
TNF-Family receptors in immune homeostasis and diseaseZ01AR041133 · NIAMS · NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES · PI SIEGEL, RICHARD M · 2002 to 2008
$2.6M
Medical Research Council G0400720
6 · The paper itself

Abstract

TNF receptor-associated periodic syndrome (TRAPS) is a dominantly inherited disease caused by missense mutations in the TNF receptor 1 (TNFR1) gene. Patients suffer from periodic bouts of severe abdominal pain, localised inflammation, migratory rashes, and fever. More than 40 individual mutations have been identified, all of which occur in the extracellular domain of TNFR1. In the present review we discuss new findings describing aberrant trafficking and function of TNFR1 harbouring TRAPS mutations, challenging the hypothesis that TRAPS pathology is driven by defective receptor shedding, and we suggest that TNFR1 might acquire novel functions in the endoplasmic reticulum, distinct from its role as a cell surface receptor. We also describe the clinical manifestations of TRAPS, current treatment regimens, and the widening array of patient mutations.

Indexed as

Mutation, MissenseProtein FoldingEndoplasmic ReticulumFamilial Mediterranean FeverHumansReceptors, Tumor Necrosis Factor, Type ISignal TransductionReceptors, Tumor Necrosis Factor, Type I

Identifiers

PMID17666110
PMCPMC2206363
OpenAlexW2097962902

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.