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Nucleotide-binding oligomerization domain containing 2

NOD2, CARD15, Blau
This gene is a member of the Nod1/Apaf-1 family and encodes a protein with two caspase recruitment (CARD) domains and six leucine-rich repeats (LRRs). The protein is primarily expressed in the peripheral blood leukocytes. It plays a role in the immune response to intracellular bacterial lipopolysaccharides (LPS) by recognizing the muramyl dipeptide (MDP) derived from them and activating the NFKB protein. Mutations in this gene have been associated with Crohn disease and Blau syndrome. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: NOD, Nod1, CAN, IBD, HAD
Papers on NOD2
NOD2 Is Regulated By Mir-320 in Physiological Conditions but this Control Is Altered in Inflamed Tissues of Patients with Inflammatory Bowel Disease.
Stronati et al., Roma, Italy. In Inflamm Bowel Dis, Feb 2016
In the present study, we speculated that miR-320 controls NOD2 (nucleotide-binding oligomerization domain) expression, because it contains multiple binding sites in the 3'-untranslated region of the gene.
ORF3 of Hepatitis E Virus Inhibits the Expression of Proinflammatory Cytokines and Chemotactic Factors in LPS-Stimulated Human PMA-THP1 Cells by Inhibiting NF-κB Pathway.
Zhang et al., Chongqing, China. In Viral Immunol, Feb 2016
Further study showed that mRNA and protein levels of pattern recognition receptors (PRRs), such as Toll-like receptor 4 (TLR4), TNF receptor-associated factor 6 (TRAF6), and nucleotide-binding oligomerization domain containing 2 (NOD2), decreased after infection of pLL3.7-ORF3
Granulomatous skin involvement in a patient with an unusual NOD2 mutation.
Smith et al., Boston, United States. In Australas J Dermatol, Feb 2016
Blau syndrome has been linked to encoding mutations in the NOD-2 gene and is inherited in an autosomal dominant form.
Beyond the Inflammasome: Regulatory NLR Modulation of the Host Immune Response Following Virus Exposure.
Allen et al., Moldova. In J Gen Virol, Feb 2016
Regulatory NLRs that augment pro-inflammatory pathways include NOD1 and NOD2, which have been shown to form a multi-protein complex termed the NODosome that significantly modulates interferon and NF-κB signaling following viral infection.
Next generation sequencing revealed DNA ligase IV deficiency in a "developmentally normal" patient with massive brain Epstein-Barr virus-positive diffuse large B-cell lymphoma.
Aleinikova et al., Minsk, Belarus. In Clin Immunol, Feb 2016
RESULT: We identified three heterozygous mutations in LIG4 gene c.2736+3delC and c.8 C>T (p.A3V) inherited from mother and c.26C>T (p.T9I) - from father after PID panel sequencing and some additional polymorphisms in ATM, NOD2 and NLRP3 genes.
The microbiome and its implications in intestinal transplantation.
Fishbein et al., Al Manşūrah, Egypt. In Curr Opin Organ Transplant, Feb 2016
RECENT FINDINGS: Recent findings highlight the importance of Paneth cells as crucial producers of antimicrobial peptides that control the intestinal host-microbial interface as well as the essential role of NOD2 as a master regulator of antimicrobial host defenses.
Genetic variants associated with drugs-induced immediate hypersensitivity reactions: a PRISMA-compliant systematic review.
Task force “Genetic predictors of drug hypersensitivity” of the European Network on Drug Allergy (ENDA) of EAACI. et al., Vandœuvre-lès-Nancy, France. In Allergy, Jan 2016
Genes involved in IR to betalactams belonged to HLA type 2 antigen processing, IgE-production, atopy and inflammation, including 4 genes validated by replications, HLA-DRA, ILR4, NOD2 and LGALS3.
Migraine Triggers and Oxidative Stress: A Narrative Review and Synthesis.
Borkum, United States. In Headache, Jan 2016
BACKGROUND: Blau theorized that migraine triggers are exposures that in higher amounts would damage the brain.
Dysbiotic gut microbiome: A key element of Crohn's disease.
Sipos et al., Budapest, Hungary. In Comp Immunol Microbiol Infect Dis, Dec 2015
The presence of Crohn's-associated variants of NOD2 and ATG16L genes appears to be associated not only with alterations of mucosal barrier functions, and bacterial killing, but the gut microbiota, as well, reflecting a potential relationship between the host's genotype and intestinal dysbiosis, involved in disease etiology.
Expression of Nucleotide-oligomerization Domain (NOD) and Related Genes in Mouse Tissues Infected with Mycobacterium leprae.
Kang et al., Seoul, South Korea. In Immune Netw, Dec 2015
The mRNA expression of NOD1, NOD2, caspase-1 and ASC was increased in mouse footpads.
Inherited determinants of Crohn's disease and ulcerative colitis phenotypes: a genetic association study.
Lees et al., Cambridge, United Kingdom. In Lancet, Nov 2015
Three loci (NOD2, MHC, and MST1 3p21) were associated with subphenotypes of inflammatory bowel disease, mainly disease location (essentially fixed over time; median follow-up of 10·5 years).
Association analyses identify 38 susceptibility loci for inflammatory bowel disease and highlight shared genetic risk across populations.
IBD Genetics Consortium et al., Groningen, Netherlands. In Nat Genet, Sep 2015
Nevertheless, we observe genetic heterogeneity between divergent populations at several established risk loci driven by differences in allele frequency (NOD2) or effect size (TNFSF15 and ATG16L1) or a combination of these factors (IL23R and IRGM).
NOD1 and NOD2: signaling, host defense, and inflammatory disease.
Núñez et al., Ann Arbor, United States. In Immunity, 2015
The nucleotide-binding oligomerization domain (NOD) proteins NOD1 and NOD2, the founding members of the intracellular NOD-like receptor family, sense conserved motifs in bacterial peptidoglycan and induce proinflammatory and antimicrobial responses.
Pattern recognition receptor signaling in human dendritic cells is enhanced by ICOS ligand and modulated by the Crohn's disease ICOSLG risk allele.
Abraham et al., New Haven, United States. In Immunity, 2014
Homotypic interactions between the costimulatory molecule ICOS and the ICOS ligand on MDDCs amplified nucleotide-binding oligomerization domain 2 (NOD2)-initiated cytokine secretion.
Endosomes are specialized platforms for bacterial sensing and NOD2 signalling.
Mellman et al., San Francisco, United States. In Nature, 2014
Internalized pathogens also activate sensors in the cytosol such as NOD1 and NOD2 (ref.
Nod2 improves barrier function of intestinal epithelial cells via enhancement of TLR responses.
den Haan et al., Amsterdam, Netherlands. In Mol Immunol, 2012
studies indicate that Nod2 stimulation by MDP enhances TLR-mediated intestinal epithelial cell barrier function and chemokine production; failure of this protective mechanism may contribute to increased risk of Crohn's disease in individuals with a loss-of-function mutation in NOD2
The c-Jun N-terminal kinase (JNK)-binding protein (JNKBP1) acts as a negative regulator of NOD2 protein signaling by inhibiting its oligomerization process.
Legrand-Poels et al., Liège, Belgium. In J Biol Chem, 2012
JNKBP1 and NOD2 are co-expressed in the human intestinal epithelium and in immune cells recruited in the lamina propria, which suggests that JNKBP1 contributes to maintain NOD2-mediated intestinal immune homeostasis.
A dual role for receptor-interacting protein kinase 2 (RIP2) kinase activity in nucleotide-binding oligomerization domain 2 (NOD2)-dependent autophagy.
McDonald et al., Cleveland, United States. In J Biol Chem, 2012
RIP2 tyrosine kinase activity is not only required for NOD2-dependent autophagy but plays a dual role in this process.
The ubiquitin ligase XIAP recruits LUBAC for NOD2 signaling in inflammation and innate immunity.
Gyrd-Hansen et al., Copenhagen, Denmark. In Mol Cell, 2012
the RING domain of XIAP is essential for NOD2 signaling
Muramyl dipeptide induces NOD2-dependent Ly6C(high) monocyte recruitment to the lungs and protects against influenza virus infection.
Gosselin et al., Québec, Canada. In Plos One, 2011
Muramyl dipeptide induces NOD2-dependent Ly6C(high) monocyte recruitment to the lungs and protects against influenza virus infection
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