Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Association between anti-tumour necrosis factor treatment response and genetic variants within the TLR and NF{kappa}B signalling pathways.

Annals of the rheumatic diseases - 1 Jul 2010

Potter Catherine, Cordell Heather J, Barton Anne, Daly Ann K, Hyrich Kimme L, Mann Derek A, Morgan Ann W, Wilson Anthony G, Isaacs John D

Abstract excerpt

OBJECTIVE: To determine whether genetic variation within genes integral to the Toll-like receptor (TLR) and NFkappaB signalling systems, two cardinal regulators of inflammatory and immune responses, contributes towards the observed variation in response to tumour necrosis factor (TNF) blocking ag...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Adalimumab
Share to Antibodies, Monoclonal, Humanized

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Antirheumatic Agents

Share to Epidemiologic Methods

Share to Etanercept

Share to Infliximab

Share to Receptors, Tumor Necrosis Factor

Share to Toll-Like Receptors

Source

Identifiers

PMID: 20448286
DOI: 10.1136/ard.2009.117309

Genes

TNF
CHUK

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 2 Sept 2026. Prepared record publication-20448286-2026-09-02.2. Manifest publication-graph-cohort-2026-09-02.2.

Source receipt: PubMed via Helena Literature Corpus, retrieved 2 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Association between anti-tumour necrosis factor treatment response and genetic variants within the TLR and NF{kappa}B signalling pathways.PMID 20448286Read ↗

Genetic Variations in Pattern Recognition Receptor Loci Are Associated with Anti-TNF Response in Patients with Rheumatoid Arthritis.Semantic proximity Read ↗

Genetic variants within the MAP kinase signalling network and anti-TNF treatment response in rheumatoid arthritis patients.Semantic proximity Read ↗

Genome-wide association study of genetic predictors of anti-tumor necrosis factor treatment efficacy in rheumatoid arthritis identifies associations with polymorphisms at seven loci.Semantic proximity Read ↗

Confirmation of an IRAK3 polymorphism as a genetic marker predicting response to anti-TNF treatment in rheumatoid arthritis.Semantic proximity Read ↗

Genetic variants that predict response to anti-tumor necrosis factor therapy in rheumatoid arthritis: current challenges and future directionsSemantic proximity Read ↗

Anti-TNF treatment response in rheumatoid arthritis patients is associated with genetic variation in the NLRP3-inflammasome.Semantic proximity Read ↗

Systematic review and meta-analysis: pharmacogenetics of anti-TNF treatment response in rheumatoid arthritis.Semantic proximity Read ↗

Investigation of single nucleotide polymorphisms and biological pathways associated with response to TNFα inhibitors in patients with rheumatoid arthritis.Semantic proximity Read ↗

Rheumatoid arthritis risk allele PTPRC is also associated with response to anti-tumor necrosis factor alpha therapy.Semantic proximity Read ↗

Investigation of genetic variants within candidate genes of the TNFRSF1B signalling pathway on the response to anti-TNF agents in a UK cohort of rheumatoid arthritis patients.Semantic proximity Read ↗

Genome-wide association analysis of anti-TNF drug response in patients with rheumatoid arthritis.Semantic proximity Read ↗

Genetic variants in toll-like receptors are not associated with rheumatoid arthritis susceptibility or anti-tumour necrosis factor treatment outcome.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.