Evidence map›Paper›PMID 25520185›Full record

ReviewOpen biology2014

Insights into the molecular basis of the NOD2 signalling pathway.

Joseph P Boyle, Rhiannon Parkhouse, Tom P Monie

Open access · goldAbstract readReview
In one paragraph

Review in Open biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
5.6field-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

51 citing papers in PubMed, 102 citations in OpenAlex.

  1. Multi-omics characterization of Yao syndrome identifies three pathophysiological axes and disease-specific divergence from Blau syndrome.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Ripks and Neuroinflammation.Molecular neurobiology · 2024
    Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Aging · 2021
    Article
  19. Revisiting peptidoglycan sensing: interactions with host immunity and beyond.Chemical communications (Cambridge, England) · 2020
    Review
  20. Chitotriosidase: a marker and modulator of lung disease.European respiratory review : an official journal of the European Respiratory Society · 2020
    Review
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 1 country.

Joseph P BoyleDepartment of Biochemistry, University of Cambridge, Cambridge, UK Department of Veterinary Medicine, University of Cambridge, Cambridge, UK.
Rhiannon ParkhouseDepartment of Biochemistry, University of Cambridge, Cambridge, UK.
Tom P MonieDepartment of Veterinary Medicine, University of Cambridge, Cambridge, UK MRC Human Nutrition Research, Elsie Widdowson Laboratory, 120 Fulbourn Road, Cambridge, UK tpm22@cam.ac.uk.
University of Cambridge · GBMRC Human Nutrition Research · GB

Funding

Biotechnology and Biological Sciences Research CouncilWellcome Trust WT085090MA
6 · The paper itself

Abstract

The cytosolic pattern recognition receptor NOD2 is activated by the peptidoglycan fragment muramyl dipeptide to generate a proinflammatory immune response. Downstream effects include the secretion of cytokines such as interleukin 8, the upregulation of pro-interleukin 1β, the induction of autophagy, the production of antimicrobial peptides and defensins, and contributions to the maintenance of the composition of the intestinal microbiota. Polymorphisms in NOD2 are the cause of the inflammatory disorder Blau syndrome and act as susceptibility factors for the inflammatory bowel condition Crohn's disease. The complexity of NOD2 signalling is highlighted by the observation that over 30 cellular proteins interact with NOD2 directly and influence or regulate its functional activity. Previously, the majority of reviews on NOD2 function have focused upon the role of NOD2 in inflammatory disease or in its interaction with and response to microbes. However, the functionality of NOD2 is underpinned by its biochemical interactions. Consequently, in this review, we have taken the opportunity to address the more 'basic' elements of NOD2 signalling. In particular, we have focused upon the core interactions of NOD2 with protein factors that influence and modulate the signal transduction pathways involved in NOD2 signalling. Further, where information exists, such as in relation to the role of RIP2, we have drawn comparison with the closely related, but functionally discrete, pattern recognition receptor NOD1. Overall, we provide a comprehensive resource targeted at understanding the complexities of NOD2 signalling.

Indexed as

Signal TransductionAnimalsArthritisAutophagyCranial Nerve DiseasesCrohn DiseaseGene Expression RegulationHereditary Autoinflammatory DiseasesHumansImmunity, InnateIntestinal MucosaIntestinesNod1 Signaling Adaptor ProteinNod2 Signaling Adaptor ProteinSarcoidosisSynovitisNOD1 protein, humanNod1 Signaling Adaptor ProteinNOD2 protein, humanNod2 Signaling Adaptor Proteininnate immunityNLRNOD1/2post-translational modificationRIP2 kinasesignal transduction

Identifiers

PMID25520185
PMCPMC4281710
OpenAlexW2102292063

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.