{"database":"BioModels","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Pdf":["https://www.ebi.ac.uk/biomodels/model/download/MODEL4780181279?filename=MODEL4780181279.pdf"],"Svg":["https://www.ebi.ac.uk/biomodels/model/download/MODEL4780181279?filename=MODEL4780181279.svg"],"Owl":["https://www.ebi.ac.uk/biomodels/model/download/MODEL4780181279?filename=MODEL4780181279-biopax2.owl","https://www.ebi.ac.uk/biomodels/model/download/MODEL4780181279?filename=MODEL4780181279-biopax3.owl"],"Xml":["https://www.ebi.ac.uk/biomodels/model/download/MODEL4780181279?filename=MODEL4780181279_urn.xml","https://www.ebi.ac.uk/biomodels/model/download/MODEL4780181279?filename=MODEL4780181279_url.xml"],"Other":["https://www.ebi.ac.uk/biomodels/model/download/MODEL4780181279?filename=MODEL4780181279.sci","https://www.ebi.ac.uk/biomodels/model/download/MODEL4780181279?filename=MODEL4780181279.png","https://www.ebi.ac.uk/biomodels/model/download/MODEL4780181279?filename=MODEL4780181279.xpp","https://www.ebi.ac.uk/biomodels/model/download/MODEL4780181279?filename=MODEL4780181279.m","https://www.ebi.ac.uk/biomodels/model/download/MODEL4780181279?filename=MODEL4780181279.vcml"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"scores":null,"additional":{"submitter":["Sharat Vayttaden"],"curationStatus":["Non-curated"],"modellingApproach":["ordinary differential equation model"],"levelVersion":["L2V1"],"full_dataset_link":["https://www.ebi.ac.uk/biomodels/MODEL4780181279"],"publication_pubmed":["11466441"],"isPrivate":["false"],"repository":["BioModels"],"modelFormat":["SBML"],"omics_type":["Models"],"tokenised_name":["Kuroda2001 NO cGMP Pathway"],"publication_year":["2001"],"submissionId":["MODEL4780181279"],"modelFlag":["Non Miriam"],"publication_authors":["Shinya Kuroda, N Schweighofer, M Kawato"],"first_author":["Shinya Kuroda"],"publication":["11466441,\n                            Because multiple molecular signal transduction pathways regulate cerebellar long-term depression (LTD), which is thought to be a possible molecular and cellular basis of cerebellar learning, the systematic relationship between cerebellar LTD and the currently known signal transduction pathways remains obscure. To address this issue, we built a new diagram of signal transduction pathways and developed a computational model of kinetic simulation for the phosphorylation of AMPA receptors, known as a key step for expressing cerebellar LTD. The phosphorylation of AMPA receptors in this model consists of an initial phase and an intermediate phase. We show that the initial phase is mediated by the activation of linear cascades of protein kinase C (PKC), whereas the intermediate phase is mediated by a mitogen-activated protein (MAP) kinase-dependent positive feedback loop pathway that is responsible for the transition from the transient phosphorylation of the AMPA receptors to the stable phosphorylation of the AMPA receptors. These phases are dually regulated by the PKC and protein phosphatase pathways. Both phases also require nitric oxide (NO), although NO per se does not show any ability to induce LTD; this is consistent with a permissive role as reported experimentally (Lev-Ram et al., 1997). Therefore, the kinetic simulation is a powerful tool for understanding and exploring the behaviors of complex signal transduction pathways involved in cerebellar LTD.. 15, 21.\n                            Kawato Dynamic Brain Project, ERATO, Japan Science and Technology, Kyoto 619-0288, Japan. kshinya@erato.atr.co.jp"],"submitter_mail":["doqcs@ncbs.res.in"],"submitter_affiliation":["DOQCS"],"pubmed_abstract":["Because multiple molecular signal transduction pathways regulate cerebellar long-term depression (LTD), which is thought to be a possible molecular and cellular basis of cerebellar learning, the systematic relationship between cerebellar LTD and the currently known signal transduction pathways remains obscure. To address this issue, we built a new diagram of signal transduction pathways and developed a computational model of kinetic simulation for the phosphorylation of AMPA receptors, known as a key step for expressing cerebellar LTD. The phosphorylation of AMPA receptors in this model consists of an initial phase and an intermediate phase. We show that the initial phase is mediated by the activation of linear cascades of protein kinase C (PKC), whereas the intermediate phase is mediated by a mitogen-activated protein (MAP) kinase-dependent positive feedback loop pathway that is responsible for the transition from the transient phosphorylation of the AMPA receptors to the stable phosphorylation of the AMPA receptors. These phases are dually regulated by the PKC and protein phosphatase pathways. Both phases also require nitric oxide (NO), although NO per se does not show any ability to induce LTD; this is consistent with a permissive role as reported experimentally (Lev-Ram et al., 1997). Therefore, the kinetic simulation is a powerful tool for understanding and exploring the behaviors of complex signal transduction pathways involved in cerebellar LTD."],"pubmed_title":["Exploration of signal transduction pathways in cerebellar long-term depression by kinetic simulation."],"pubmed_authors":["Kuroda S S, Schweighofer N N, Kawato M M"],"additional_accession":[]},"is_claimable":false,"name":"Kuroda2001_NO_cGMP_Pathway","description":"\n      \n    This model of sGC is based on the paper by    Kuroda S. et al. J Neurosci. (2001) 21(15):5693-702\n        . This models features the activation of sGC by NO, synthesis of cGMP, activity of PKG and PP2A in the synapse. The rates and concentrations have been taken from literature. It contains only the part described in figure 1B of the article.    This model originates from BioModels Database: A Database of Annotated Published Models. 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":"2009-10-08","publication":"2005-01-01","submission":"2008-09-10"},"accession":"MODEL4780181279","cross_references":{"pubmed":["11466441"],"biomodels__db":["MODEL4780181279"],"go":["GO:0048167"],"taxonomy":["9606"],"bto":["BTO:0000232"]}}