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dc.contributor.authorRichard, Guilhemen_US
dc.contributor.authorBelta, Calinen_US
dc.contributor.authorAmar, Salomonen_US
dc.contributor.authorJulius, A. Agungen_US
dc.coverage.spatialUnited Statesen_US
dc.date2012-01-06
dc.date.accessioned2018-06-26T18:09:09Z
dc.date.available2018-06-26T18:09:09Z
dc.date.issued2012
dc.identifierhttps://www.ncbi.nlm.nih.gov/pubmed/22363624
dc.identifier.citationGuilhem Richard, Calin Belta, A Agung Julius, Salomon Amar. 2012. "Controlling the outcome of the Toll-like receptor signaling pathways.." PLoS One, v. 7, issue 2, p. e31341
dc.identifier.issn1932-6203
dc.identifier.urihttps://hdl.handle.net/2144/29718
dc.description.abstractThe Toll-Like Receptors (TLRs) are proteins involved in the immune system that increase cytokine levels when triggered. While cytokines coordinate the response to infection, they appear to be detrimental to the host when reaching too high levels. Several studies have shown that the deletion of specific TLRs was beneficial for the host, as cytokine levels were decreased consequently. It is not clear, however, how targeting other components of the TLR pathways can improve the responses to infections. We applied the concept of Minimal Cut Sets (MCS) to the ihsTLR v1.0 model of the TLR pathways to determine sets of reactions whose knockouts disrupt these pathways. We decomposed the TLR network into 34 modules and determined signatures for each MCS, i.e. the list of targeted modules. We uncovered 2,669 MCS organized in 68 signatures. Very few MCS targeted directly the TLRs, indicating that they may not be efficient targets for controlling these pathways. We mapped the species of the TLR network to genes in human and mouse, and determined more than 10,000 Essential Gene Sets (EGS). Each EGS provides genes whose deletion suppresses the network's outputs.en_US
dc.description.sponsorshipR01 DE015989 - NIDCR NIH HHS; R01DE015989-S1 - NIDCR NIH HHSen_US
dc.format.extentp. e31341en_US
dc.languageeng
dc.relation.ispartofPLoS One
dc.rightsAttribution 4.0 Internationalen_US
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/
dc.subjectHumansen_US
dc.subjectMiceen_US
dc.subjectScience & technologyen_US
dc.subjectMultidisciplinary sciencesen_US
dc.subjectNF-Kappa-Ben_US
dc.subjectEscherichia colien_US
dc.subjectTranscriptional regulationen_US
dc.subjectMetabolismen_US
dc.subjectInfectionen_US
dc.subjectNetworksen_US
dc.subjectDiseaseen_US
dc.subjectModelsen_US
dc.subjectGenomeen_US
dc.subjectFamilyen_US
dc.subjectAnimalsen_US
dc.subjectGenes, essentialen_US
dc.subjectModels, biologicalen_US
dc.subjectReactive oxygen speciesen_US
dc.subjectReproducibility of resultsen_US
dc.subjectSignal transductionen_US
dc.subjectToll-like receptorsen_US
dc.subjectMD multidisciplinaryen_US
dc.titleControlling the outcome of the Toll-like receptor signaling pathwaysen_US
dc.typeArticleen_US
dc.identifier.doi10.1371/journal.pone.0031341
dc.rights.licenseCC-BYen_US
pubs.elements-sourcepubmeden_US
pubs.notesEmbargo: Not knownen_US
pubs.organisational-groupBoston Universityen_US
pubs.organisational-groupBoston University, College of Engineeringen_US
pubs.organisational-groupBoston University, College of Engineering, Department of Mechanical Engineeringen_US
pubs.publication-statusPublisheden_US


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Attribution 4.0 International
Except where otherwise noted, this item's license is described as Attribution 4.0 International