Evidence map›Paper›PMID 30837326›Full record

ReviewBioscience reports2019

NOD-like receptors: major players (and targets) in the interface between innate immunity and cancer.

Fernando J Velloso, Marina Trombetta-Lima, Valesca Anschau, Mari C Sogayar, Ricardo G Correa

Open access · goldAbstract readReview
In one paragraph

Review in Bioscience reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers.

0numbers the graph read from it
0cells of the map it votes in
77citing papers in PubMed
5.8field-weighted citation impact, top 3% 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

77 citing papers in PubMed, 132 citations in OpenAlex.

  1. Review
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  9. Observational
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  12. The cancer microbiome.Advances in clinical chemistry · 2025
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17 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

5 authors at 4 institutions in 3 countries.

Fernando J VellosoDepartment of Pharmacology, Physiology and Neuroscience, Rutgers-New Jersey Medical School Newark, NJ, U.S.A. fernando.velloso@rutgers.edu rcorrea@sbpdiscovery.org.ORCID 0000-0002-5582-2912
Marina Trombetta-LimaCell and Molecular Therapy Center (NUCEL), Internal Medicine Department, School of Medicine, University of São Paulo (USP), São Paulo, SP, Brazil.
Valesca AnschauInstitute for Integrative Systems Biology (I2SysBio), Universitat de Valencia-CSIC, Valencia 46980, Spain.
Mari C SogayarCell and Molecular Therapy Center (NUCEL), Internal Medicine Department, School of Medicine, University of São Paulo (USP), São Paulo, SP, Brazil.
Ricardo G CorreaNCI-Designated Cancer Center, Sanford Burnham Prebys Medical Discovery Institute, La Jolla, CA, U.S.A. fernando.velloso@rutgers.edu rcorrea@sbpdiscovery.org.ORCID 0000-0001-6940-7034
Universidade de São Paulo · BRDiscovery Institute · USRutgers, The State University of New Jersey · USUniversitat de València · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Innate immunity comprises several inflammation-related modulatory pathways which receive signals from an array of membrane-bound and cytoplasmic pattern recognition receptors (PRRs). The NLRs (NACHT (NAIP (neuronal apoptosis inhibitor protein), C2TA (MHC class 2 transcription activator), HET-E (incompatibility locus protein from Podospora anserina) and TP1 (telomerase-associated protein) and Leucine-Rich Repeat (LRR) domain containing proteins) relate to a large family of cytosolic innate receptors, involved in detection of intracellular pathogens and endogenous byproducts of tissue injury. These receptors may recognize pathogen-associated molecular patterns (PAMPs) and/or danger-associated molecular patterns (DAMPs), activating host responses against pathogen infection and cellular stress. NLR-driven downstream signals trigger a number of signaling circuitries, which may either initiate the formation of inflammasomes and/or activate nuclear factor κB (NF-κB), stress kinases, interferon response factors (IRFs), inflammatory caspases and autophagy. Disruption of those signals may lead to a number of pro-inflammatory conditions, eventually promoting the onset of human malignancies. In this review, we describe the structures and functions of the most well-defined NLR proteins and highlight their association and biological impact on a diverse number of cancers.

Indexed as

Immunity, InnateAnimalsHumansInflammasomesInflammationNeoplasmsNF-kappa BNLR ProteinsPathogen-Associated Molecular Pattern MoleculesReceptors, Pattern RecognitionInflammasomesNF-kappa BNLR ProteinsPathogen-Associated Molecular Pattern MoleculesReceptors, Pattern RecognitioncancerinflammasomeNF-kBNLRNOD1NOD2

Identifiers

PMID30837326
PMCPMC6454022
OpenAlexW2920215789

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.