Disease Score gda Association Type Type Original DB Sentence supporting the association PMID PMID Year
CUI: C0021390
Disease: Inflammatory Bowel Diseases
Inflammatory Bowel Diseases
0.500 AlteredExpression group LHGDN Together with the mutation-derived truncation and functional change of the NOD2 protein, this could be part of the complex pathophysiology of barrier disruption as it is observed in inflammatory bowel diseases. 12671897 2003
CUI: C0021390
Disease: Inflammatory Bowel Diseases
Inflammatory Bowel Diseases
0.500 AlteredExpression group BEFREE The present study aims at investigating the interplay between autophagy, NOD2 and AIEC bacteria and assessing the expression level of autophagic proteins in intestinal biopsies of pediatric patients with inflammatory bowel disease (IBD). 27335178 2016
CUI: C0021390
Disease: Inflammatory Bowel Diseases
Inflammatory Bowel Diseases
0.500 AlteredExpression group BEFREE This finding might provide us with a novel therapeutic target for inflammatory bowel disease to inhibit IL-23p19 over-expression via the NOD2-c-Rel pathway. 27563808 2016
CUI: C0021390
Disease: Inflammatory Bowel Diseases
Inflammatory Bowel Diseases
0.500 AlteredExpression group BEFREE MiR-320 and NOD2 expression were analyzed in mucosal samples of 40 children with inflammatory bowel disease. 26752466 2016
CUI: C0021390
Disease: Inflammatory Bowel Diseases
Inflammatory Bowel Diseases
0.500 AlteredExpression group BEFREE Subsequently, KEGG generated bacterial TLR4 and NOD2 transcriptional signatures strongly associated with inflamed IBD transcriptomes and with the Mito-0 signature as determined by Spearman's analysis (coefficient of correlation, r = 0.92, p < .05). 31063017 2019
CUI: C0021390
Disease: Inflammatory Bowel Diseases
Inflammatory Bowel Diseases
0.500 AlteredExpression group BEFREE These studies thus suggest that NOD1- or NOD2-independenent activation of RICK plays a major role in both murine experimental colitis and human IBD. 31132297 2019
CUI: C0021390
Disease: Inflammatory Bowel Diseases
Inflammatory Bowel Diseases
0.500 Biomarker group BEFREE Caspase recruitment domain (CARD) family (CARD9, CARD10, CARD11, CARD14 and CARD15) are increased during active inflammation in patients with inflammatory bowel disease. 30008619 2018
CUI: C0021390
Disease: Inflammatory Bowel Diseases
Inflammatory Bowel Diseases
0.500 Biomarker group BEFREE Since IL-4 regulation and expression are abnormal in IBD, the IL4R gene is thus both a positional and functional candidate for IBD1. 10663555 2000
CUI: C0021390
Disease: Inflammatory Bowel Diseases
Inflammatory Bowel Diseases
0.500 Biomarker group BEFREE Because CARD4/NOD1 shares many structural and functional similarities with CARD15, we tested its putative role in IBD. 12477763 2003
CUI: C0021390
Disease: Inflammatory Bowel Diseases
Inflammatory Bowel Diseases
0.500 Biomarker group BEFREE ASCA were analysed in 98 twin pairs with inflammatory bowel disease and were related to clinical phenotype and CARD15/NOD2 genotype. 15863472 2005
CUI: C0021390
Disease: Inflammatory Bowel Diseases
Inflammatory Bowel Diseases
0.500 Biomarker group CTD_human Deep resequencing of GWAS loci identifies independent rare variants associated with inflammatory bowel disease. 21983784 2011
CUI: C0021390
Disease: Inflammatory Bowel Diseases
Inflammatory Bowel Diseases
0.500 Biomarker group BEFREE Genetics of inflammatory bowel disease: beyond NOD2. 28404137 2017
CUI: C0021390
Disease: Inflammatory Bowel Diseases
Inflammatory Bowel Diseases
0.500 Biomarker group BEFREE We conclude that gene expression profiling of mucosal biopsies from the descending colon of patients with CD could not be correlated with CARD15 status or with familial disposition for IBD. 17410442 2007
CUI: C0021390
Disease: Inflammatory Bowel Diseases
Inflammatory Bowel Diseases
0.500 Biomarker group BEFREE Single nucleotide polymorphisms (SNPs) in genes involved in bacterial recognition, CARD15 and TLR4, increased the risk of inflammatory bowel disease (IBD) in a New Zealand Caucasian case-control cohort. 19275920 2009
CUI: C0021390
Disease: Inflammatory Bowel Diseases
Inflammatory Bowel Diseases
0.500 Biomarker group BEFREE This review seeks to examine the current knowledge regarding the regulation of this family of receptors and their signalling pathways as well as how their expression changes in disease states with particular focus on NOD1 and NOD2 in inflammatory bowel diseases among others. 27706808 2017
CUI: C0021390
Disease: Inflammatory Bowel Diseases
Inflammatory Bowel Diseases
0.500 Biomarker group BEFREE Genetic mutations in the innate immune receptor nucleotide-binding oligomerization domain-containing 2 (Nod2) have demonstrated increased susceptibility to Crohn's disease, an inflammatory bowel disease that is hypothesized to be accompanied by changes in the gut microbiota. 27748583 2017
CUI: C0021390
Disease: Inflammatory Bowel Diseases
Inflammatory Bowel Diseases
0.500 Biomarker group BEFREE Association between polymorphisms in the Toll-like receptor 4, CD14, and CARD15/NOD2 and inflammatory bowel disease in the Greek population. 15655821 2005
CUI: C0021390
Disease: Inflammatory Bowel Diseases
Inflammatory Bowel Diseases
0.500 Biomarker group BEFREE Large consortia contributed to the elucidation of the genetics, for instance, of IBD identifying a number of genes involved in innate mucosal defense and immune tolerance (most prominent, e.g., NOD2) and other related processes. 28895120 2017
CUI: C0021390
Disease: Inflammatory Bowel Diseases
Inflammatory Bowel Diseases
0.500 Biomarker group BEFREE Some IBD associated genes are involved in innate immunity, in the autophagy and in the inflammatory response such as NOD2, ATG16L1 and IL23R, while other are implicated in immune mediated disease (STAT3) and in susceptibility to mycobacterium infection (IL12B). 26604638 2015
CUI: C0021390
Disease: Inflammatory Bowel Diseases
Inflammatory Bowel Diseases
0.500 Biomarker group BEFREE In this review, we introduce past, current, and possible future concepts for IBD models regarding T helper (Th) 1, Th2, and Th17, antigen sampling and presentation, regulatory cell networks, NOD2, Toll-like receptors, bacteria/epithelia interaction, stem cells, autophagy, microRNAs, and glycoimmunology, and we also discuss the relevance of these new concepts, developed at the bench (in animal models), to the bedside. 18297430 2008
CUI: C0021390
Disease: Inflammatory Bowel Diseases
Inflammatory Bowel Diseases
0.500 Biomarker group BEFREE The discovery that several genes linked to IBD modulate microbial recognition and innate immune pathways, such as nucleotide oligomerization domain 2 (Nod2), and genes that mediate autophagy (ie, ATG16L1, IRGM), has highlighted the critical role of host-microbe interactions in controlling intestinal immune homeostasis. 22955361 2012
CUI: C0021390
Disease: Inflammatory Bowel Diseases
Inflammatory Bowel Diseases
0.500 Biomarker group BEFREE Disease concordance, zygosity, and NOD2/CARD15 status: follow-up of a population-based cohort of Danish twins with inflammatory bowel disease. 16279904 2005
CUI: C0021390
Disease: Inflammatory Bowel Diseases
Inflammatory Bowel Diseases
0.500 Biomarker group BEFREE A significant role for CARD15/NOD2 gene in predisposition to SpA was ruled out, in agreement with the hypothesis that the inflammatory bowel disease in SpA is determined by factors different than those responsible for isolated Crohn's disease. 12951869 2003
CUI: C0021390
Disease: Inflammatory Bowel Diseases
Inflammatory Bowel Diseases
0.500 Biomarker group BEFREE Genetic polymorphisms present in IL10, IL23R, NOD2, and ATG16L1 associated with susceptibility to inflammatory bowel disease in Mexican population. 31651650 2020
CUI: C0021390
Disease: Inflammatory Bowel Diseases
Inflammatory Bowel Diseases
0.500 Biomarker group CTD_human Thus, in a two-hit hypothesis, decreased barrier function due to dysfunctional mitochondrial is amplified by lack of NOD2 in transporting enterocytes: subsequently, greater numbers of bacteria entering the mucosa would be a significant inflammatory threat especially since individuals with NOD2 mutations have compromised macrophage and Paneth cell responses to bacteria.<b>NEW & NOTEWORTHY</b> Increased internalization of bacteria by epithelia with dysfunctional mitochondria (reduced ATP) is potentiated if the cells lack nucleotide-binding oligomerization domain 2 (NOD2), mutations in which are inflammatory bowel disease-susceptibility traits. 28450277 2017