{"database":"BioModels","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Pdf":["https://www.ebi.ac.uk/biomodels/model/download/MODEL1150151512?filename=MODEL1150151512.pdf"],"Svg":["https://www.ebi.ac.uk/biomodels/model/download/MODEL1150151512?filename=MODEL1150151512.svg"],"Owl":["https://www.ebi.ac.uk/biomodels/model/download/MODEL1150151512?filename=MODEL1150151512-biopax3.owl","https://www.ebi.ac.uk/biomodels/model/download/MODEL1150151512?filename=MODEL1150151512-biopax2.owl"],"Xml":["https://www.ebi.ac.uk/biomodels/model/download/MODEL1150151512?filename=MODEL1150151512_url.xml","https://www.ebi.ac.uk/biomodels/model/download/MODEL1150151512?filename=MODEL1150151512_urn.xml"],"Other":["https://www.ebi.ac.uk/biomodels/model/download/MODEL1150151512?filename=MODEL1150151512.sci","https://www.ebi.ac.uk/biomodels/model/download/MODEL1150151512?filename=MODEL1150151512.png","https://www.ebi.ac.uk/biomodels/model/download/MODEL1150151512?filename=MODEL1150151512.xpp","https://www.ebi.ac.uk/biomodels/model/download/MODEL1150151512?filename=MODEL1150151512.vcml","https://www.ebi.ac.uk/biomodels/model/download/MODEL1150151512?filename=MODEL1150151512.m"]},"type":"primary"},"statusCodeValue":200,"statusCode":"OK"}],"scores":null,"additional":{"submitter":["Arne Gjuvsland"],"curationStatus":["Non-curated"],"modellingApproach":["ordinary differential equation model"],"levelVersion":["L2V3"],"full_dataset_link":["https://www.ebi.ac.uk/biomodels/MODEL1150151512"],"publication_pubmed":["15142845"],"isPrivate":["false"],"repository":["BioModels"],"modelFormat":["SBML"],"omics_type":["Models"],"tokenised_name":["Bondarenko2004 Myocyte AP apical"],"publication_year":["2004"],"submissionId":["MODEL1150151512"],"publication_authors":["Vladimir E Bondarenko, Gyula P Szigeti, Glenna C L Bett, Song-Jung Kim, Randall L Rasmusson"],"first_author":["Vladimir E Bondarenko"],"publication":["15142845,\n                            We have developed a mathematical model of the mouse ventricular myocyte action potential (AP) from voltage-clamp data of the underlying currents and Ca2+ transients. Wherever possible, we used Markov models to represent the molecular structure and function of ion channels. The model includes detailed intracellular Ca2+ dynamics, with simulations of localized events such as sarcoplasmic Ca2+ release into a small intracellular volume bounded by the sarcolemma and sarcoplasmic reticulum. Transporter-mediated Ca2+ fluxes from the bulk cytosol are closely matched to the experimentally reported values and predict stimulation rate-dependent changes in Ca2+ transients. Our model reproduces the properties of cardiac myocytes from two different regions of the heart: the apex and the septum. The septum has a relatively prolonged AP, which reflects a relatively small contribution from the rapid transient outward K+ current in the septum. The attribution of putative molecular bases for several of the component currents enables our mouse model to be used to simulate the behavior of genetically modified transgenic mice.. 3, 287.\n                            Department of Physiology and Biophysics, School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, Buffalo, New York 14214-3078, USA."],"submitter_mail":["arne.gjuvsland@umb.no"],"submitter_affiliation":["Norwegian University of Life Science"],"pubmed_abstract":["We have developed a mathematical model of the mouse ventricular myocyte action potential (AP) from voltage-clamp data of the underlying currents and Ca2+ transients. Wherever possible, we used Markov models to represent the molecular structure and function of ion channels. The model includes detailed intracellular Ca2+ dynamics, with simulations of localized events such as sarcoplasmic Ca2+ release into a small intracellular volume bounded by the sarcolemma and sarcoplasmic reticulum. Transporter-mediated Ca2+ fluxes from the bulk cytosol are closely matched to the experimentally reported values and predict stimulation rate-dependent changes in Ca2+ transients. Our model reproduces the properties of cardiac myocytes from two different regions of the heart: the apex and the septum. The septum has a relatively prolonged AP, which reflects a relatively small contribution from the rapid transient outward K+ current in the septum. The attribution of putative molecular bases for several of the component currents enables our mouse model to be used to simulate the behavior of genetically modified transgenic mice."],"pubmed_title":["Computer model of action potential of mouse ventricular myocytes."],"pubmed_authors":["Bondarenko Vladimir E VE, Szigeti Gyula P GP, Bett Glenna C L GC, Kim Song-Jung SJ, Rasmusson Randall L RL"],"additional_accession":[]},"is_claimable":false,"name":"Bondarenko2004_Myocyte_AP_apical","description":"\n      \n        This the model from the article:      \n        Computer model of action potential of mouse ventricular myocytes.\n        \n          Bondarenko VE, Szigeti GP, Bett GC, Kim SJ, Rasmusson RL      Am. J. Physiol. Heart Circ. Physiol.\n          2004 Sep;287(3):H1378-403. Pubmed ID:      15142845\n          , \n      doi:      10.1152/ajpheart.00185.2003\n          .      \n        Abstract:\n        \n          We have developed a mathematical model of the mouse ventricular myocyte action potential (AP) from voltage-clamp data of the underlying currents and Ca      2+\n          transients. Wherever possible, we used Markov models to represent the molecular structure and function of ion channels. The model includes detailed intracellular Ca      2+\n          dynamics, with simulations of localized events such as sarcoplasmic Ca      2+\n          release into a small intracellular volume bounded by the sarcolemma and sarcoplasmic reticulum. Transporter-mediated Ca      2+\n          fluxes from the bulk cytosol are closely matched to the experimentally reported values and predict stimulation rate-dependent changes in Ca      2+\n          transients. Our model reproduces the properties of cardiac myocytes from two different regions of the heart: the apex and the septum. The septum has a relatively prolonged AP, which reflects a relatively small contribution from the rapid transient outward K      +\n          current in the septum. The attribution of putative molecular bases for several of the component currents enables our mouse model to be used to simulate the behavior of genetically modified transgenic mice.      \n      This SBML model has been converted from a CellML model (see:      Bondarenko 2004 vers. 5 var. 1\n          ) in the      CellML repository\n          .      \n          It has been slightly changed and a parameter E_try been introduced to make it valid SBML. The CellML model was orginally created by:      \n          James Lawson      \n          Auckland Bioengineering Institute      \n          j.lawson(at)auckland.ac.nz      \n      \n          From the original CellML model:      \n          The      original CellML model version\n          \"has been curated by Penny Noble from Oxford University  and is known to run in COR and PCEnv. This model represents the APICAL CELL variant as described in Bondarenko et al.'s 2004 paper and all units are consistent. The model is able to reproduce the action potential traces from Figure 16 of the publication. This model has a PCEnv session file associated with it.\"      \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  \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":"2012-02-02","publication":"2005-01-01","submission":"2009-03-23"},"accession":"MODEL1150151512","cross_references":{"pubmed":["15142845"],"biomodels__db":["MODEL1150151512"],"go":["GO:0086017"],"taxonomy":["10090"],"bto":["BTO:0002320"]}}