<HashMap><database>BioModels</database><file_versions><headers><Content-Type>application/xml</Content-Type></headers><body><files><Txt>https://www.ebi.ac.uk/biomodels/model/download/BIOMD0000000125?filename=curation_notes.txt</Txt><Pdf>https://www.ebi.ac.uk/biomodels/model/download/BIOMD0000000125?filename=BIOMD0000000125.pdf</Pdf><Svg>https://www.ebi.ac.uk/biomodels/model/download/BIOMD0000000125?filename=BIOMD0000000125.svg</Svg><Owl>https://www.ebi.ac.uk/biomodels/model/download/BIOMD0000000125?filename=BIOMD0000000125-biopax2.owl</Owl><Owl>https://www.ebi.ac.uk/biomodels/model/download/BIOMD0000000125?filename=BIOMD0000000125-biopax3.owl</Owl><Xml>https://www.ebi.ac.uk/biomodels/model/download/BIOMD0000000125?filename=manifest.xml</Xml><Xml>https://www.ebi.ac.uk/biomodels/model/download/BIOMD0000000125?filename=BIOMD0000000125_url.xml</Xml><Other>https://www.ebi.ac.uk/biomodels/model/download/BIOMD0000000125?filename=curation_image.png</Other><Other>https://www.ebi.ac.uk/biomodels/model/download/BIOMD0000000125?filename=BIOMD0000000125.m</Other><Other>https://www.ebi.ac.uk/biomodels/model/download/BIOMD0000000125?filename=BIOMD0000000125.png</Other><Other>https://www.ebi.ac.uk/biomodels/model/download/BIOMD0000000125?filename=BIOMD0000000125.ode</Other><Other>https://www.ebi.ac.uk/biomodels/model/download/BIOMD0000000125?filename=BIOMD0000000125-matlab.m</Other><Other>https://www.ebi.ac.uk/biomodels/model/download/BIOMD0000000125?filename=BIOMD0000000125_url.sedml</Other><Other>https://www.ebi.ac.uk/biomodels/model/download/BIOMD0000000125?filename=BIOMD0000000125.vcml</Other><Other>https://www.ebi.ac.uk/biomodels/model/download/BIOMD0000000125?filename=metadata.rdf</Other></files><type>primary</type></body><statusCode>OK</statusCode><statusCodeValue>200</statusCodeValue></file_versions><scores/><additional><submitter>Enuo He</submitter><curationStatus>Manually curated</curationStatus><modellingApproach>ordinary differential equation model</modellingApproach><levelVersion>L2V1</levelVersion><full_dataset_link>https://www.biomodels.org/BIOMD0000000125</full_dataset_link><publication_pubmed>16729058</publication_pubmed><isPrivate>false</isPrivate><repository>BioModels</repository><modelFormat>SBML</modelFormat><omics_type>Models</omics_type><tokenised_name>Komarova2005 TheoreticalFramework BasicArchitecture</tokenised_name><publication_year>2005</publication_year><submissionId>MODEL2451230486</submissionId><publication_authors>Natalia L Komarova, Xiufen Zou, Qing Nie, Lee Bardwell</publication_authors><first_author>Natalia L Komarova</first_author><publication>16729058,
                            Different cellular signal transduction pathways are often interconnected, so that the potential for undesirable crosstalk between pathways exists. Nevertheless, signaling networks have evolved that maintain specificity from signal to cellular response. Here, we develop a framework for the analysis of networks containing two or more interconnected signaling pathways. We define two properties, specificity and fidelity, that all pathways in a network must possess in order to avoid paradoxical situations where one pathway activates another pathway's output, or responds to another pathway's input, more than its own. In unembellished networks that share components, it is impossible for all pathways to have both mutual specificity and mutual fidelity. However, inclusion of either of two related insulating mechanisms--compartmentalization or the action of a scaffold protein--allows both properties to be achieved, provided deactivation rates are fast compared to exchange rates.. null, 1.
                            Department of Mathematics, University of California, Irvine, CA 92697, USA. komarova@uci.edu</publication><submitter_mail>enuo.he@wolfson.ox.ac.uk</submitter_mail><submitter_affiliation>University of Oxford</submitter_affiliation><publicationId>BIOMD0000000125</publicationId><pubmed_abstract>Different cellular signal transduction pathways are often interconnected, so that the potential for undesirable crosstalk between pathways exists. Nevertheless, signaling networks have evolved that maintain specificity from signal to cellular response. Here, we develop a framework for the analysis of networks containing two or more interconnected signaling pathways. We define two properties, specificity and fidelity, that all pathways in a network must possess in order to avoid paradoxical situations where one pathway activates another pathway's output, or responds to another pathway's input, more than its own. In unembellished networks that share components, it is impossible for all pathways to have both mutual specificity and mutual fidelity. However, inclusion of either of two related insulating mechanisms--compartmentalization or the action of a scaffold protein--allows both properties to be achieved, provided deactivation rates are fast compared to exchange rates.</pubmed_abstract><pubmed_title>A theoretical framework for specificity in cell signaling.</pubmed_title><pubmed_authors>Komarova Natalia L NL, Zou Xiufen X, Nie Qing Q, Bardwell Lee L</pubmed_authors><pubmed_title_synonyms>Taf[[II]]250, Taf200, dTAF[[II]]230, TAF[[II]]250, d230, dTAF[[II]]250, TAF[[II]]230, TFIID TAF250, cel, cell, TAF200, l(3)84Ab, dTAFII250, Taf1p, TAF[II]250, BG:DS00004.13, TAFII-250, CG17603, TAF250/230, TAF[[II]], EfW1, Cell, dTAF230, dTAF250, dmTAF[[II]]230, TAFII250, DmelCG17603, signalling process, Taf250, dmTAF1, SR3-5, Taf230, p230, TAF[[II]]250/230, TFIID, TAF, TAF230, single organism signaling., TAF250, TAF1</pubmed_title_synonyms><pubmed_abstract_synonyms>signal transduction by protein phosphorylation, reactivity, Signal Transduction Systems, Signal Transductions, Pathway, determination, System, Receptor-Mediated, STK10, signal transduction by conformational transition, Signal, Receptor-Mediated Signal Transductions, Pathways, Signal Transduction System, FASTK, Signal Pathways, Signal Transduction Pathway, signal transduction by trans-phosphorylation, Receptor Mediated Signal Transduction, Signal Transduction, signaling cascade, signalling pathway, signaling pathway, signalling process, ATP:Fas-activated serine/threonine protein phosphotransferase activity, Receptor-Mediated Signal Transduction, responsivity, Systems, chemical analysis, signal transduction by cis-phosphorylation, Signal Transduction Pathways, Transductions, assay, response, Cell Signaling, signalling cascade, Transduction, Signal Pathway, Fast., FAST, single organism signaling</pubmed_abstract_synonyms><description_synonyms>extent, scale tissue, dTAF[[II]]230, TAF[[II]]250, d230, biological signaling, Sectors, Public Sectors, Papers, YB, completeness, DmelCG2706, peltate hair, AUTSX5, number, TAF200, DXS648, l(3)84Ab, dTAFII250, Copyrights, BG:DS00004.13, NOVH, TAFII-250, TAF250/230, CCN3, EfW1, QM, Cell, presence., dTAF230, dmTAF[[II]]230, count in organism, TAFII250, Yb, dmTAF1, IGFBP-9, Taf230, Public, Public Domain, p230, Domains, TAF[[II]]250/230, TFIID, NOV, scales, Public Enterprise, Enterprises, PlexA1, CG2706, Domain, fs(1)M104, Data Base, TAF250, Taf[[II]]250, Taf200, figures, Plxn1, dTAF[[II]]250, TAF[[II]]230, TFIID TAF250, scale, cel, cell, plant peltate hair, Public Domains, nov, Taf1p, TAF[II]250, IGFBP9, CG17603, Public Enterprises, TAF[[II]], mKIAA4053, fs(1)Y[b], signalling, IBP-9, dTAF250, Kiaa4053, DmelCG17603, Sector, signalling process, Taf250, L10, SR3-5, signaling process, C130088N23Rik, EG:95B7.8, 2600013D04Rik, PLXN1, DXS648E, NOVh, TAF, Enterprise, TAF230, single organism signaling, TAF1</description_synonyms></additional><is_claimable>false</is_claimable><name>Komarova2005_TheoreticalFramework_BasicArchitecture</name><description>
      
        This model according to the paper      A Theoretical Framework for Specificity in Cell Signalling
          The model is "basic architecture" of Figure2A. Figure2B, Figure2C have been reproduced by MathSBML. The reproduced figures are slightly different from the original ones in the paper, the peak of [x2] is higher than 1 and is not decreasing dramatically when [x0]=0. And I think maybe the author shift the or scale the curves.      
            
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            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.
                
            
      
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