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HIV slow progressors with variants in the TLR and NOD2 pathways showed reduced pro-inflammatory responses compared to matched controls. Low-range plasma levels of fibronectin was observed in a LTNP harboring two FN1 variants.
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The antimicrobial actions of PALA required expression of nucleotide-binding, oligomerization domain 2 (NOD2), receptor-interacting serine/threonine-protein kinase 2 (RIP2), and carbamoyl phosphatase synthase II/aspartate transcarbamylase/dihydroorotase (CAD).
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This study demonstrates for the first time that NOD2 expression and pathway activation are aberrant in YAOS syndrome, and specific NOD2 genotypes result in distinct NOD2 expression and cytokine profiles.
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study exemplifies how targeting of the ATP-binding pocket in RIPK2 can be exploited to interfere with the RIPK2-XIAP interaction for modulation of NOD signaling.
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NOD2 genotypes were not associated with microbial composition and diversity.
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NOD2 is crucial to control intracellular infection caused by Leishmania spp. NOD2 receptor is important for Leishmania recognition, the control of intracellular killing, and the induction of innate and adaptive immune responses.
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NOD1 and NOD2 mRNA was constitutively expressed in both tumor and adjacent healthy renal tissue, with NOD1 being significantly lower and in contrast NOD2 significantly higher expressed in tumor tissue compared to healthy tissues.
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poor clinical healing outcome was associated with increased local expression of the pattern recognition receptor NOD2
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A rare and, not yet, reported missense variation of the NOD2 gene, N1010K, was detected and co-segregated across affected patients. In silico evaluation and modelling highlighted evidence for an adverse effect of the N1010K variation with regard to Crohn's Disease (CD).
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The frequency of NOD2/CARD15 gene mutations is high in Crohn's disease (CD) and ulcerative colitis among Bedouin Arab IBD patients and is associated with younger age at onset in CD and male gender.
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NOD2 has unique expression sites in salivary glands, and they may synergistically activate autophagy in salivary glands under conditions of inflammation.
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In this well-controlled study of NOD2 genotype and fecal microbiota, we identified no significant genotype-microbiota associations in Crohn's Disease patients
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The aim of this study was to identify how genetic testing (NOD2/CARD15) can be used in patients with Crohn's disease to predict the need for surgical treatment.
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The results support a role of guanylate cyclase C signaling and disturbed electrolyte homeostasis in development of IBD. Furthermore, downregulation of metallothioneins in the ileal mucosa of familial GUCY2C diarrhea syndrome patients may contribute to inflammatory bowel disease development, possibly alongside effects from NOD2 risk variants.
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Mutations in the NOD2 gene are associated with a specific phenotype and lower anti-tumor necrosis factor trough levels in Crohn's disease.
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In cirrhosis patients with ascites NOD2 gene variants were associated with an increased cumulative probability of spontaneous bacterial peritonitis (SBP) compared to wild-type. In cirrhosis, functional polymorphisms of Pattern recognition receptors did not improve the identification of patients with high risk of bacterial infections beyond SBP or progressive diseases course.
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Study results showed no association between the single nucleotide polymorphism rs8057341 in NOD2 and leprosy in Brazilian population.
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This first study on genetic susceptibility in sclerosing cholangitis in critically ill patients patients shows an extraordinary high frequency of NOD2 variation, pointing to a critical role of inherited impaired anti-bacterial defense in the development of this devastating biliary disease.
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NOD1 and NOD2 expression and induced release of pro-inflammatory mediators were impaired in infants, contributing to the high susceptibility of infants to infection
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NOD2 caspase recruitment domains (CARDs) bind to one end of the RIP2 CARD filament