IntAct European Bioinformatics Institute IntAct intact http://www.ebi.ac.uk/ http://www.ebi.ac.uk/intact/query/${ac} EBI-[0-9]+|IA:[0-9]+ INTerAction database (IntAct) provides an open source database and toolkit for the storage, presentation and analysis of molecular interactions. http://www.ebi.ac.uk/intact European Bioinformatics Institute; Wellcome Trust Genome Campus; Hinxton, Cambridge; CB10 1SD; United Kingdom http://www.ebi.ac.uk/intact/ http://www.ebi.ac.uk/ aldhous-2010-1 human-sw480 Human SW480 adenocarcinoma cell line sw480 SW480- human primary colorectal adenocarcinoma cell line There is a G -> A mutation in codon 273 of the p53 gene resulting in an Arg -> His substitution and a C -> T mutation in codon 309 resulting in a Pro -> Ser substitution. http://www.atcc.org/ATCCAdvancedCatalogSearch/ProductDetails/tabid/452/Default.aspx?ATCCNum=CCL-228&Template=cellBiology anti tag coip anti tag coimmunoprecipitation anti tag coip western blot western blot Immuno blot Immuno blot Aldhous MC., Soo K., Stark LA., Ulanicka AA., Easterbrook JE., Dunlop MG., Satsangi J. Cigarette Smoke Extract (CSE) Myc-tagged NOD2 was identified to be human in other publication from the same corresponding author (PMID:22684479) maldhous@ed.ac.uk PloS one 2010 imex curation Only protein-protein interactions imex curation nod2_human Nucleotide-binding oligomerization domain-containing protein 2 IBD1 NOD2 CARD15 Caspase recruitment domain-containing protein 15 Inflammatory bowel disease protein 1 protein protein human Homo sapiens Human MGEEGGSASHDEEERASVLLGHSPGCEMCSQEAFQAQRSQLVELLVSGSLEGFESVLDWLLSWEVLSWEDYEGFHLLGQPLSHLARRLLDTVWNKGTWACQKLIAAAQEAQADSQSPKLHGCWDPHSLHPARDLQSHRPAIVRRLHSHVENMLDLAWERGFVSQYECDEIRLPIFTPSQRARRLLDLATVKANGLAAFLLQHVQELPVPLALPLEAATCKKYMAKLRTTVSAQSRFLSTYDGAETLCLEDIYTENVLEVWADVGMAGPPQKSPATLGLEELFSTPGHLNDDADTVLVVGEAGSGKSTLLQRLHLLWAAGQDFQEFLFVFPFSCRQLQCMAKPLSVRTLLFEHCCWPDVGQEDIFQLLLDHPDRVLLTFDGFDEFKFRFTDRERHCSPTDPTSVQTLLFNLLQGNLLKNARKVVTSRPAAVSAFLRKYIRTEFNLKGFSEQGIELYLRKRHHEPGVADRLIRLLQETSALHGLCHLPVFSWMVSKCHQELLLQEGGSPKTTTDMYLLILQHFLLHATPPDSASQGLGPSLLRGRLPTLLHLGRLALWGLGMCCYVFSAQQLQAAQVSPDDISLGFLVRAKGVVPGSTAPLEFLHITFQCFFAAFYLALSADVPPALLRHLFNCGRPGNSPMARLLPTMCIQASEGKDSSVAALLQKAEPHNLQITAAFLAGLLSREHWGLLAECQTSEKALLRRQACARWCLARSLRKHFHSIPPAAPGEAKSVHAMPGFIWLIRSLYEMQEERLARKAARGLNVGHLKLTFCSVGPTECAALAFVLQHLRRPVALQLDYNSVGDIGVEQLLPCLGVCKALYLRDNNISDRGICKLIECALHCEQLQKLALFNNKLTDGCAHSMAKLLACRQNFLALRLGNNYITAAGAQVLAEGLRGNTSLQFLGFWGNRVGDEGAQALAEALGDHQSLRWLSLVGNNIGSVGAQALALMLAKNVMLEELCLEENHLQDEGVCSLAEGLKKNSSLKILKLSNNCITYLGAEALLQALERNDTILEVWLRGNTFSLEEVDKLGCRDTRLLL mint homomint Induces NF-kappa-B via RICK (CARDIAK, RIP2) and IKK-gamma. Confers responsiveness to intracellular bacterial lipopolysaccharides (LPS) Defects in NOD2 are the cause of Blau syndrome (BS) [MIM:186580]. BS is a rare autosomal dominant disorder characterized by early-onset granulomatous arthritis, uveitis and skin rash Defects in NOD2 are a cause of susceptibility to Crohn disease (CD) [MIM:266600]. CD is a form of remitting inflammatory bowel disease (IBD). CD may involve any part of the gastrointestinal tract, but most frequently the terminal ileum and colon. Bowel inflammation is transmural and discontinuous. Crohn disease is commonly classified as autoimmune disease Defects in NOD2 are a cause of susceptibility to ulcerative colitis [MIM:191390]. It is a chronic inflammatory bowel disease. In ulcerative colitis, the inflammation is continuous and limited to rectal and colonic mucosal layers. Ulcerative colitis is commonly classified as autoimmune disease Defects in NOD2 are the cause of early-onset sarcoidosis (EOS) [MIM:609464]. Sarcoidosis is a multiorganic inflammatory disease with unknown etiology, characterized by the histologic features of non-caseating epithelioid granulomas. In childhood, 2 distinct types of sarcoidosis have been described. Usually the disease is detected in older children by chest radiography and the clinical manifestations are characterized by a classical triad of lung, lymph node, and eye involvement, similar to those in adults. In contrast, early-onset sarcoidosis (EOS), which usually appears in those younger than 4 years of age, is quite rare and has a distinct triad of skin, joint, and eye disorders, without apparent pulmonary involvement. Compared with an asymptomatic and sometimes naturally disappearing course of the disease in older children, EOS is progressive and in many cases causes severe complications, such as blindness, joint destruction, and visceral involvement ripk2_human Receptor-interacting serine/threonine-protein kinase 2 RIPK2 CARDIAK RICK RIP2 UNQ277/PRO314/PRO34092 RIP-like-interacting CLARP kinase Receptor-interacting protein 2 CARD-containing interleukin-1 beta-converting enzyme-associated kinase Tyrosine-protein kinase RIPK2 protein protein human Homo sapiens Human MNGEAICSALPTIPYHKLADLRYLSRGASGTVSSARHADWRVQVAVKHLHIHTPLLDSERKDVLREAEILHKARFSYILPILGICNEPEFLGIVTEYMPNGSLNELLHRKTEYPDVAWPLRFRILHEIALGVNYLHNMTPPLLHHDLKTQNILLDNEFHVKIADFGLSKWRMMSLSQSRSSKSAPEGGTIIYMPPENYEPGQKSRASIKHDIYSYAVITWEVLSRKQPFEDVTNPLQIMYSVSQGHRPVINEESLPYDIPHRARMISLIESGWAQNPDERPSFLKCLIELEPVLRTFEEITFLEAVIQLKKTKLQSVSSAIHLCDKKKMELSLNIPVNHGPQEESCGSSQLHENSGSPETSRSLPAPQDNDFLSRKAQDCYFMKLHHCPGNHSWDSTISGSQRAAFCDHKTTPCSSAIINPLSTAGNSERLQPGIAQQWIQSKREDIVNQMTEACLNQSLDALLSRDLIMKEDYELVSTKPTRTSKVRQLLDTTDIQGEEFAKVIVQKLKDNKQMGLQPYPEILVVSRSPSLNLLQNKSM nod2-ripk2-3 3487806 N/A 3487807 anti tag western anti tag western blot anti tag western unspecified role unspecified role bait bait over-expressed over expressed level over-expressed living cell living cell myc tag myc tag myc tag EUKLISEED epitope tag EUKLISEED epitope tag undetermined undetermined sequence position undetermined undetermined undetermined sequence position undetermined false N/A 3487808 unspecified role unspecified role prey prey living cell living cell physiological level physiological level endogenous level endogenous endogenous endogenous level physical association physical association false false false Fig. 3 At 8 hours there was no significant difference in the amount of NOD2-myc/RIPK2 complex in the cells treated with different stimuli, whereas after 18 hours cells treated with T and TN had smaller amounts of NOD2-myc/RIPK2 complex compared with cells treated with TC and TCN (figure 3A, representative blots of CoIPs for 8 and 18 hours; fig. 3B for densitometry against RIPK2 for 18 hours, from 3 experiments). For unstimulated cells and those stimulated with C, N and CN there was little change in the amount of NOD2-myc/RIPK2 complex. At 18 hours, the relative amounts of NOD2-myc/RIPK2 in cells stimulated with T, TC, TN and TCN were significantly different (Friedman test, p = 0.0330).