{"database":"BioModels","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Pdf":["https://www.ebi.ac.uk/biomodels/model/download/MODEL2463683119?filename=MODEL2463683119.pdf"],"Svg":["https://www.ebi.ac.uk/biomodels/model/download/MODEL2463683119?filename=MODEL2463683119.svg"],"Owl":["https://www.ebi.ac.uk/biomodels/model/download/MODEL2463683119?filename=MODEL2463683119-biopax2.owl","https://www.ebi.ac.uk/biomodels/model/download/MODEL2463683119?filename=MODEL2463683119-biopax3.owl"],"Xml":["https://www.ebi.ac.uk/biomodels/model/download/MODEL2463683119?filename=MODEL2463683119_urn.xml","https://www.ebi.ac.uk/biomodels/model/download/MODEL2463683119?filename=MODEL2463683119_url.xml"],"Other":["https://www.ebi.ac.uk/biomodels/model/download/MODEL2463683119?filename=MODEL2463683119.xpp","https://www.ebi.ac.uk/biomodels/model/download/MODEL2463683119?filename=MODEL2463683119.sci","https://www.ebi.ac.uk/biomodels/model/download/MODEL2463683119?filename=MODEL2463683119.png","https://www.ebi.ac.uk/biomodels/model/download/MODEL2463683119?filename=MODEL2463683119.vcml","https://www.ebi.ac.uk/biomodels/model/download/MODEL2463683119?filename=MODEL2463683119.m"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"scores":null,"additional":{"submitter":["Molecular Systems Biology"],"curationStatus":["Non-curated"],"levelVersion":["L2V1"],"full_dataset_link":["https://www.ebi.ac.uk/biomodels/MODEL2463683119"],"publication_pubmed":["16738560"],"isPrivate":["false"],"repository":["BioModels"],"modelFormat":["SBML"],"omics_type":["Models"],"tokenised_name":["Oda2006 TollLikeR"],"publication_year":["2006"],"submissionId":["MODEL2463683119"],"modelFlag":["Non Kinetic"],"publication_authors":["Kanae Oda, Hiroaki Kitano"],"first_author":["Kanae Oda"],"publication":["16738560,\n                            Recognition of pathogen-associated molecular signatures is critically important in proper activation of the immune system. The toll-like receptor (TLR) signaling network is responsible for innate immune response. In mammalians, there are 11 TLRs that recognize a variety of ligands from pathogens to trigger immunological responses. In this paper, we present a comprehensive map of TLRs and interleukin 1 receptor signaling networks based on papers published so far. The map illustrates the possible existence of a main network subsystem that has a bow-tie structure in which myeloid differentiation primary response gene 88 (MyD88) is a nonredundant core element, two collateral subsystems with small GTPase and phosphatidylinositol signaling, and MyD88-independent pathway. There is extensive crosstalk between the main bow-tie network and subsystems, as well as feedback and feedforward controls. One obvious feature of this network is the fragility against removal of the nonredundant core element, which is MyD88, and involvement of collateral subsystems for generating different reactions and gene expressions for different stimuli.. null, 2.\n                            The Systems Biology Institute, Shibuya, Tokyo, Japan."],"submitter_mail":["msbforum@embo.org"],"submitter_affiliation":["Nature Publishing Group"],"pubmed_abstract":["Recognition of pathogen-associated molecular signatures is critically important in proper activation of the immune system. The toll-like receptor (TLR) signaling network is responsible for innate immune response. In mammalians, there are 11 TLRs that recognize a variety of ligands from pathogens to trigger immunological responses. In this paper, we present a comprehensive map of TLRs and interleukin 1 receptor signaling networks based on papers published so far. The map illustrates the possible existence of a main network subsystem that has a bow-tie structure in which myeloid differentiation primary response gene 88 (MyD88) is a nonredundant core element, two collateral subsystems with small GTPase and phosphatidylinositol signaling, and MyD88-independent pathway. There is extensive crosstalk between the main bow-tie network and subsystems, as well as feedback and feedforward controls. One obvious feature of this network is the fragility against removal of the nonredundant core element, which is MyD88, and involvement of collateral subsystems for generating different reactions and gene expressions for different stimuli."],"pubmed_title":["A comprehensive map of the toll-like receptor signaling network."],"pubmed_authors":["Oda Kanae K, Kitano Hiroaki H"],"additional_accession":[]},"is_claimable":false,"name":"Oda2006_TollLikeR","description":"\n      \n        This model originates from BioModels Database: A Database of Annotated Published Models (http://www.ebi.ac.uk/biomodels/). It is copyright (c) 2005-2011 The BioModels.net Team.      \n          To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to      CC0 Public Domain Dedication\n          for more information.      \n      In summary, you are entitled to use this encoded model in absolutely any manner you deem suitable, verbatim, or with modification, alone or embedded it in a larger context, redistribute it, commercially or not, in a restricted way or not..      \n      \n          To cite BioModels Database, please use:      Li C, Donizelli M, Rodriguez N, Dharuri H, Endler L, Chelliah V, Li L, He E, Henry A, Stefan MI, Snoep JL, Hucka M, Le Novère N, Laibe C (2010) BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models. BMC Syst Biol., 4:92.\n  \n\n","dates":{"last_modification":"2007-09-04","publication":"2005-01-01","submission":"2006-11-02"},"accession":"MODEL2463683119","cross_references":{"pubmed":["16738560"],"biomodels__db":["MODEL2463683119"],"go":["GO:0002224"],"taxonomy":["40674"]}}