{"database":"BioModels","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Pdf":["https://www.ebi.ac.uk/biomodels/model/download/MODEL1405070000?filename=MODEL1405070000.pdf"],"Owl":["https://www.ebi.ac.uk/biomodels/model/download/MODEL1405070000?filename=MODEL1405070000-biopax3.owl","https://www.ebi.ac.uk/biomodels/model/download/MODEL1405070000?filename=MODEL1405070000-biopax2.owl"],"Svg":["https://www.ebi.ac.uk/biomodels/model/download/MODEL1405070000?filename=MODEL1405070000.svg"],"Xml":["https://www.ebi.ac.uk/biomodels/model/download/MODEL1405070000?filename=MODEL1405070000_url.xml","https://www.ebi.ac.uk/biomodels/model/download/MODEL1405070000?filename=MODEL1405070000_urn.xml"],"Other":["https://www.ebi.ac.uk/biomodels/model/download/MODEL1405070000?filename=MODEL1405070000.sci","https://www.ebi.ac.uk/biomodels/model/download/MODEL1405070000?filename=MODEL1405070000.png","https://www.ebi.ac.uk/biomodels/model/download/MODEL1405070000?filename=MODEL1405070000.xpp","https://www.ebi.ac.uk/biomodels/model/download/MODEL1405070000?filename=MODEL1405070000.m","https://www.ebi.ac.uk/biomodels/model/download/MODEL1405070000?filename=MODEL1405070000.vcml"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"scores":null,"additional":{"submitter":["Andrew Dolan"],"curationStatus":["Non-curated"],"modellingApproach":["ordinary differential equation model"],"levelVersion":["L2V1"],"full_dataset_link":["https://www.ebi.ac.uk/biomodels/MODEL1405070000"],"publication_pubmed":["24806937"],"isPrivate":["false"],"repository":["BioModels"],"modelFormat":["SBML"],"omics_type":["Models"],"tokenised_name":["Dolan2014   calcium homeostasis (SOCE)"],"publication_year":["2014"],"submissionId":["MODEL1405070000"],"publication_authors":["Andrew T Dolan, Scott L Diamond"],"first_author":["Andrew T Dolan"],"publication":["24806937,\n                            Resting platelets maintain a stable level of low cytoplasmic calcium ([Ca(2+)]cyt) and high dense tubular system calcium ([Ca(2+)]dts). During thrombosis, activators cause a transient rise in inositol trisphosphate (IP3) to trigger calcium mobilization from stores and elevation of [Ca(2+)]cyt. Another major source of [Ca(2+)]cyt elevation is store-operated calcium entry (SOCE) through plasmalemmal calcium channels that open in response to store depletion as [Ca(2+)]dts drops. A 34-species systems model employed kinetics describing IP3-receptor, DTS-plasmalemma puncta formation, SOCE via assembly of STIM1 and Orai1, and the plasmalemma and sarco/endoplasmic reticulum Ca(2+)-ATPases. Four constraints were imposed: calcium homeostasis before activation; stable in zero extracellular calcium; IP3-activatable; and functional SOCE. Using a Monte Carlo method to sample three unknown parameters and nine initial concentrations in a 12-dimensional space near measured or expected values, we found that model configurations that were responsive to stimuli and demonstrated significant SOCE required high inner membrane electric potential (>-70 mV) and low resting IP3 concentrations. The absence of puncta in resting cells was required to prevent spontaneous store depletion in calcium-free media. Ten-fold increases in IP3 caused saturated calcium mobilization. This systems model represents a critical step in being able to predict platelets' phenotypes during hemostasis or thrombosis.. 9, 106.\n                            Institute for Medicine and Engineering, Department of Chemical and Biomolecular Engineering, University of Pennsylvania, Philadelphia, Pennsylvania."],"submitter_mail":["adolan1348@gmail.com"],"submitter_affiliation":["University of Pennsylvania"],"pubmed_abstract":["Resting platelets maintain a stable level of low cytoplasmic calcium ([Ca(2+)]cyt) and high dense tubular system calcium ([Ca(2+)]dts). During thrombosis, activators cause a transient rise in inositol trisphosphate (IP3) to trigger calcium mobilization from stores and elevation of [Ca(2+)]cyt. Another major source of [Ca(2+)]cyt elevation is store-operated calcium entry (SOCE) through plasmalemmal calcium channels that open in response to store depletion as [Ca(2+)]dts drops. A 34-species systems model employed kinetics describing IP3-receptor, DTS-plasmalemma puncta formation, SOCE via assembly of STIM1 and Orai1, and the plasmalemma and sarco/endoplasmic reticulum Ca(2+)-ATPases. Four constraints were imposed: calcium homeostasis before activation; stable in zero extracellular calcium; IP3-activatable; and functional SOCE. Using a Monte Carlo method to sample three unknown parameters and nine initial concentrations in a 12-dimensional space near measured or expected values, we found that model configurations that were responsive to stimuli and demonstrated significant SOCE required high inner membrane electric potential (>-70 mV) and low resting IP3 concentrations. The absence of puncta in resting cells was required to prevent spontaneous store depletion in calcium-free media. Ten-fold increases in IP3 caused saturated calcium mobilization. This systems model represents a critical step in being able to predict platelets' phenotypes during hemostasis or thrombosis."],"pubmed_title":["Systems modeling of Ca(2+) homeostasis and mobilization in platelets mediated by IP3 and store-operated Ca(2+) entry."],"pubmed_authors":["Dolan Andrew T AT, Diamond Scott L SL"],"additional_accession":[]},"is_claimable":false,"name":"Dolan2014 - calcium homeostasis (SOCE)","description":"No description","dates":{"last_modification":"2014-09-10","publication":"2014-09-15","submission":"2014-05-07"},"accession":"MODEL1405070000","cross_references":{"pubmed":["24806937"],"biomodels__db":["MODEL1405070000"],"go":["GO:0055074"],"taxonomy":["9606"],"bto":["BTO:0000132"]}}