Evidence map›Paper›PMID 25201319›Full record

ReviewCurrent opinion in structural biology2014

Structural mechanisms in NLR inflammasome signaling.

Bernhard C Lechtenberg, Peter D Mace, Stefan J Riedl

Open access · greenAbstract readReview
In one paragraph

Review in Current opinion in structural biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed
5.3field-weighted citation impact, top 4% 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

64 citing papers in PubMed, 111 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Review
  5. Review
  6. Sterile activation of RNA-sensing pathways in autoimmunity.Journal of molecular cell biology · 2024
    Review
  7. Article
  8. Article
  9. New Insights on NLRP3 Inflammasome: Mechanisms of Activation, Inhibition, and Epigenetic Regulation.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2024
    Review
  10. Review
  11. Article
  12. Application of pyroptosis score in the treatment and prognosis evaluation of gastric cancer.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2023
    Article
  13. Review
  14. Article
  15. Review
  16. Review
  17. Review
  18. Review
  19. Review
  20. Article

4 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

3 authors at 2 institutions in 2 countries.

Bernhard C LechtenbergPrograms on Cell Death and Survival Networks, Sanford-Burnham Medical Research Institute, 10901 North Torrey Pines Road, La Jolla, CA 92037, USA.
Peter D MaceBiochemistry Department, Otago School of Medical Sciences, University of Otago, P.O. Box 56, 710 Cumberland St., Dunedin 9054, New Zealand. Electronic address: peter.mace@otago.ac.nz.
Stefan J RiedlPrograms on Cell Death and Survival Networks, Sanford-Burnham Medical Research Institute, 10901 North Torrey Pines Road, La Jolla, CA 92037, USA. Electronic address: sriedl@sanfordburnham.org.
Sanford Burnham Prebys Medical Discovery Institute · USUniversity of Otago · NZ

Funding

Tumor Microenvironment and Cancer ImmunologyP30CA030199 · NCI · SANFORD BURNHAM PREBYS MEDICAL DISCOVERY INSTITUTE · PI ELENA B PASQUALE · 1985 to 2026
$107.2M
The Mechanism of DISC FormationR01AA017238 · NIAAA · SANFORD BURNHAM PREBYS MEDICAL DISCOVERY INSTITUTE · PI RIEDL, STEFAN J · 2008 to 2012
$2.1M
NCI NIH HHS P30 CA030199NIAAA NIH HHS R01 AA017238NIAAA NIH HHS R01AA017238
6 · The paper itself

Abstract

Members of the NOD-like receptor (NLR) family mediate the innate immune response to a wide range of pathogens, tissue damage and other cellular stresses. They achieve modulation of these signals by forming oligomeric signaling platforms, which in analogy to the apoptosome are predicted to adopt a defined oligomeric architecture and will here be referred to as NLR oligomers. Once formed, oligomers of the NLR proteins NLRP3 or NLRC4 'recruit' the adaptor protein ASC and the effector caspase-1, whereby NLRC4 can also directly interact with caspase-1. This results in large multi-protein assemblies, termed inflammasomes. Ultimately, the formation of these inflammasomes leads to the activation of caspase-1, which then processes the cytokines IL-1β and IL-18 triggering the immune response. Here we review new insights into NLR structure and implications on NLR oligomer formation as well as the nature of multi-protein inflammasomes. Of note, so dubbed 'canonical inflammasomes' can also be triggered by the NLR NLRP1b and the non-NLR protein AIM2, however the most detailed mechanistic information at hand pertains to NLRC4 while NLRP3 represents the quintessential inflammasome trigger. Thus these two NLRs are mainly used as examples in this article.

Indexed as

ApoptosomesApoptotic Protease-Activating Factor 1Calcium-Binding ProteinsCARD Signaling Adaptor ProteinsCarrier ProteinsCaspase 10Cytoskeletal ProteinsDNA-Binding ProteinsGene Expression RegulationHumansImmunity, InnateInflammasomesInterleukin-18Interleukin-1betaNLR Family, Pyrin Domain-Containing 3 ProteinProtein ConformationAIM2 protein, humanAPAF1 protein, humanApoptosomesApoptotic Protease-Activating Factor 1Calcium-Binding ProteinsCARD Signaling Adaptor ProteinsCarrier ProteinsCASP10 protein, humanCaspase 10Cytoskeletal ProteinsDNA-Binding ProteinsInflammasomesInterleukin-18Interleukin-1betaNLRC4 protein, humanNLR Family, Pyrin Domain-Containing 3 ProteinNLRP3 protein, humanPyrin

Identifiers

PMID25201319
PMCPMC4268015
OpenAlexW2042328552

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.