Cell CollectiveModelsTomas Helikarhttps://cellcollective.org/#1582/signaling-in-macrophage-activation41.53161SBML1Cell Collectivehttps://cellcollective.org/#1582:1/signaling-in-macrophage-activation<h4>Background</h4>The complex yet flexible cellular response to pathogens is orchestrated by the interaction of multiple signalling and metabolic pathways. The molecular regulation of this response has been studied in great detail but comprehensive and unambiguous diagrams describing these events are generally unavailable. Four key signalling cascades triggered early-on in the innate immune response are the toll-like receptor, interferon, NF-kappaB and apoptotic pathways, which co-operate to defend cells against a given pathogen. However, these pathways are commonly viewed as separate entities rather than an integrated network of molecular interactions.<h4>Results</h4>Here we describe the construction of a logically represented pathway diagram which attempts to integrate these four pathways central to innate immunity using a modified version of the Edinburgh Pathway Notation. The pathway map is available in a number of electronic formats and editing is supported by yEd graph editor software.<h4>Conclusion</h4>The map presents a powerful visual aid for interpreting the available pathway interaction knowledge and underscores the valuable contribution well constructed pathway diagrams make to communicating large amounts of molecular interaction data. Furthermore, we discuss issues with the limitations and scalability of pathways presented in this fashion, explore options for automated layout of large pathway networks and demonstrate how such maps can aid the interpretation of functional studies.A logic-based diagram of signalling pathways central to macrophage activation.Raza Sobia S, Robertson Kevin A KA, Lacaze Paul A PA, Page David D, Enright Anton J AJ, Ghazal Peter P, Freeman Tom C TCkappa B Enhancer Binding Protein, methionine aminopeptidase activity, NFKB-p50, nonspecific immune response, Receptors, Mbp1, sci, Social Controls, limitations, Enhancer-Binding Protein, Donor Artificial Insemination, responsivity, CDA2, HOW, How, 2, Software Engineering, study limitations, Fs(3)Hor, myd, Formal Social Controls, IKKg, Computer Program, l(3)j5D5, peptidase M activity, INSL3R, KEY, Key, Donor Artificial, adenomas, 24B, Toll Like Receptor, rabGAPLP, DmelCG2684, Immune Responses, L-methionine aminopeptidase activity, Natural, Open, stru, NF-kappa B, Computer Programs and Programming, RabGAP-5, Mbp-1, l(3)S053606, NTef2, Innate Immune Responses, ird, Nuclear Factor Kappab, CG10293, Nuclear Factor-Kappab, Non-Specific Immunity, Toll Like Receptors, Social, KBF1, l(3)j5B5, GREAT, Ig-EBP-1, RUSC3, signaling process, NF-kappaB1, Great, REL, single organism signaling, 0904/17, l(3)neo36, gyltl1b-b, Immunity, Aid., Native, MYH-associated polyposis, autosomal recessive familial adenomatous polyposis, Maps, Toll-Like Receptor, rel, results, Source Softwares, Fs(3)Sz11, Software Tools, Programs, Program, Computer Applications, DmIKKgamma, NFKB-p105, dIKK, SZ1, MDDGA6, mKIAA0609, Computer Applications Software, Kenny, Computer Applications Softwares, Heterologous Insemination, Transcription Factor NF kB, Softwares, KIAA0609, autosomal recessive, fg, LGR8, RUTBC3, Epistemology, Lgr8, Native Immunity, Software Applications, gyltl1b, p50|p105, Source Software, IKK-gamma, mdc1d, Control, expanded, RELI, Controls, Natural Resistance, early, NF kappa B Complex, RABGAP5, NF-kappa-B, Artificial Insemination, MDC1D, Applications, DmelCG16910, enr, enlarged, NF kappaB, p50/p105, Horka, multiple colorectal, CG2684, Fs(3)Horka, anon-EST:Liang-2.39, NF kB, Regulation, Innate, Interferon, Computer Software Applications, Immunoglobulin Enhancer-Binding Protein, Regulations, big, biological signaling, Innate Immunity, NF-kB, ird4, NF-kappaB, p50, Immunoglobulin, P62, relish, number, Computer, Transcription Factor, Ig EBP 1, AID, dIKK-gamma, Aid, froggy, Gyltl1a, large, DmIKK-gamma, fam:TLR, NF-KB1, DmF2, dmIKKgamma, Toll Like, Nuclear Factor kappa B, IKK[[gamma]], familial adenomatous polyposis, CG11992, MAP, Application, aid, lod, Transcription Factor NF-kB, Insemination, reactivity, Open Source Softwares, Transcription, Gpr106, l(3)s2612, Software Application, MDDGB6, familial adenomatous polyposis 2, NF-kB1, Complex, Open Source Software, RXFPR2, LARGE, Computer Software Application, autosomal recessive multiple colorectal adenomas, BPFD#36, Immune Response, IKK, Tools, Electronic, HEL-S-284, great, DmelCG10293, HIGM2, Factor-Kappab, Non Specific, GPR106, Immunoglobulin Enhancer Binding Protein, Heterologous, Applications Software, Open Source, Natural Immunity, MUTYH-Associated Polyposis, Computer Software, Formal Social Control, clone 2.39, innate immunity, qkr, Rel-p110, l(3)S090417, Cell, Tool, Human Donor, IKKgamma, Software Tool, Factor NF-kB, Social Control, KH93F, Resistance, Nuclear, Donor, p105, background, Software, NFkappaB, who, Artificial, Toll-Like, DmelCG11992, Dmikkgamma, Arp2, ARP2, Engineering, Who/How, MYH-Associated Polyposis, LGR8.1, CG16910, Lds, NF-kappa B Complex, EBP-1, introduction, signalling, Innate Immune Response, Computer Programs, Applications Softwares, signalling process, Non-Specific, cardinality, qkr[93F], MAP syndrome, regulation, Receptor, response, Rel/NF-kappaB, FAP2, colorectal adenomatous polyposisActivations, Macrophage Activations, biological signaling, Macrophage., signalling process, Logics, macrophage polarization, Activation, signaling process, single organism signaling, signalling, MacrophageActivations, Macrophage Activations, Macrophage., signalling process, macrophage polarization, Activation, single organism signaling, Macrophagekappa B Enhancer Binding Protein, methionine aminopeptidase activity, NFKB-p50, nonspecific immune response, Receptors, Mbp1, sci, Social Controls, limitations, Enhancer-Binding Protein, Donor Artificial Insemination, responsivity, CDA2, HOW, How, 2, Software Engineering, study limitations, Fs(3)Hor, myd, Formal Social Controls, IKKg, Computer Program, l(3)j5D5, peptidase M activity, INSL3R, KEY, Key, Donor Artificial, adenomas, 24B, Toll Like Receptor, rabGAPLP, DmelCG2684, Immune Responses, L-methionine aminopeptidase activity, Natural, Open, stru, NF-kappa B, Computer Programs and Programming, RabGAP-5, Mbp-1, l(3)S053606, NTef2, Innate Immune Responses, ird, Nuclear Factor Kappab, CG10293, Nuclear Factor-Kappab, Non-Specific Immunity, Toll Like Receptors, Social, KBF1, l(3)j5B5, GREAT, Ig-EBP-1, RUSC3, signaling process, NF-kappaB1, Great, REL, single organism signaling, 0904/17, l(3)neo36, gyltl1b-b, Immunity, Aid., Native, MYH-associated polyposis, autosomal recessive familial adenomatous polyposis, Maps, Toll-Like Receptor, rel, results, Source Softwares, Fs(3)Sz11, Software Tools, Programs, Program, Computer Applications, DmIKKgamma, NFKB-p105, dIKK, SZ1, MDDGA6, mKIAA0609, Computer Applications Software, Kenny, Computer Applications Softwares, Heterologous Insemination, Transcription Factor NF kB, Softwares, KIAA0609, autosomal recessive, fg, LGR8, RUTBC3, Epistemology, Lgr8, Native Immunity, Software Applications, gyltl1b, p50|p105, Source Software, IKK-gamma, mdc1d, Control, expanded, RELI, Controls, Natural Resistance, early, NF kappa B Complex, RABGAP5, NF-kappa-B, Artificial Insemination, MDC1D, Applications, DmelCG16910, enr, enlarged, NF kappaB, p50/p105, Horka, multiple colorectal, CG2684, Fs(3)Horka, anon-EST:Liang-2.39, NF kB, Regulation, Innate, Interferon, Computer Software Applications, Immunoglobulin Enhancer-Binding Protein, Regulations, big, biological signaling, Innate Immunity, NF-kB, ird4, NF-kappaB, p50, Immunoglobulin, P62, relish, number, Computer, Transcription Factor, Ig EBP 1, AID, dIKK-gamma, Aid, froggy, Gyltl1a, large, DmIKK-gamma, fam:TLR, NF-KB1, DmF2, dmIKKgamma, Toll Like, Nuclear Factor kappa B, IKK[[gamma]], familial adenomatous polyposis, CG11992, MAP, Application, aid, lod, Transcription Factor NF-kB, Insemination, reactivity, Open Source Softwares, Transcription, Gpr106, l(3)s2612, Software Application, MDDGB6, familial adenomatous polyposis 2, NF-kB1, Complex, Open Source Software, RXFPR2, LARGE, Computer Software Application, autosomal recessive multiple colorectal adenomas, BPFD#36, Immune Response, IKK, Tools, Electronic, HEL-S-284, great, DmelCG10293, HIGM2, Factor-Kappab, Non Specific, GPR106, Immunoglobulin Enhancer Binding Protein, Heterologous, Applications Software, Open Source, Natural Immunity, MUTYH-Associated Polyposis, Computer Software, Formal Social Control, clone 2.39, innate immunity, qkr, Rel-p110, l(3)S090417, Cell, Tool, Human Donor, IKKgamma, Software Tool, Factor NF-kB, Social Control, KH93F, Resistance, Nuclear, Donor, p105, background, Software, NFkappaB, who, Artificial, Toll-Like, DmelCG11992, Dmikkgamma, Arp2, ARP2, Engineering, Who/How, MYH-Associated Polyposis, LGR8.1, CG16910, Lds, NF-kappa B Complex, EBP-1, introduction, signalling, Innate Immune Response, Computer Programs, Applications Softwares, signalling process, Non-Specific, cardinality, qkr[93F], MAP syndrome, regulation, Receptor, response, Rel/NF-kappaB, FAP2, colorectal adenomatous polyposisfalseSignaling in Macrophage Activation BACKGROUND: The complex yet flexible cellular response to pathogens is orchestrated by the interaction of multiple signalling and metabolic pathways. The molecular regulation of this response has been studied in great detail but comprehensive and unambiguous diagrams describing these events are generally unavailable. Four key signalling cascades triggered early-on in the innate immune response are the toll-like receptor, interferon, NF-kappaB and apoptotic pathways, which co-operate to defend cells against a given pathogen. However, these pathways are commonly viewed as separate entities rather than an integrated network of molecular interactions. RESULTS: Here we describe the construction of a logically represented pathway diagram which attempts to integrate these four pathways central to innate immunity using a modified version of the Edinburgh Pathway Notation. The pathway map is available in a number of electronic formats and editing is supported by yEd graph editor software. CONCLUSION: The map presents a powerful visual aid for interpreting the available pathway interaction knowledge and underscores the valuable contribution well constructed pathway diagrams make to communicating large amounts of molecular interaction data. Furthermore, we discuss issues with the limitations and scalability of pathways presented in this fashion, explore options for automated layout of large pathway networks and demonstrate how such maps can aid the interpretation of functional studies.2011-09-062016-01-222016-01-22158218433497