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dc.contributor.authorRutschmann, Sophie
dc.contributor.authorJung, Alain C.
dc.contributor.authorZhou, Rui
dc.contributor.authorSilverman, Neal S.
dc.contributor.authorHoffmann, Jules A.
dc.contributor.authorFerrandon, Dominique
dc.date2022-08-11T08:09:08.000
dc.date.accessioned2022-08-23T16:18:49Z
dc.date.available2022-08-23T16:18:49Z
dc.date.issued2001-03-23
dc.date.submitted2008-12-19
dc.identifier.citationNat Immunol. 2000 Oct;1(4):342-7. <a href="http://dx.doi.org/10.1038/79801">Link to article on publisher's site</a>
dc.identifier.issn1529-2908 (Print)
dc.identifier.doi10.1038/79801
dc.identifier.pmid11017107
dc.identifier.urihttp://hdl.handle.net/20.500.14038/34903
dc.description.abstractWe have generated, by ethylmethane sulfonate mutagenesis, loss-of-function mutants in the Drosophila homolog of the mammalian I-kappa B kinase (IKK) complex component IKK gamma (also called NEMO). Our data show that Drosophila IKK gamma is required for the Relish-dependent immune induction of the genes encoding antibacterial peptides and for resistance to infections by Escherichia coli. However, it is not required for the Toll-DIF-dependent antifungal host defense. The results indicate distinct control mechanisms of the Rel-like transactivators DIF and Relish in the Drosophila innate immune response and show that Drosophila Toll does not signal through a IKK gamma-dependent signaling complex. Thus, in contrast to the vertebrate inflammatory response, IKK gamma is required for the activation of only one immune signaling pathway in Drosophila.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=11017107&dopt=Abstract">Link to Article in PubMed</a>
dc.relation.urlhttp://dx.doi.org/10.1038/79801
dc.subjectAnimals
dc.subjectAntigens, Bacterial
dc.subjectDrosophila
dc.subject*Drosophila Proteins
dc.subjectGene Expression Regulation
dc.subjectI-kappa B Kinase
dc.subjectImmunity, Natural
dc.subjectInsect Proteins
dc.subjectMembrane Glycoproteins
dc.subjectProtein-Serine-Threonine Kinases
dc.subject*Receptors, Cell Surface
dc.subjectSignal Transduction
dc.subjectToll-Like Receptors
dc.subjectTranscription Factors
dc.subjectImmunology and Infectious Disease
dc.titleRole of Drosophila IKK gamma in a toll-independent antibacterial immune response
dc.typeArticle
dc.source.journaltitleNature immunology
dc.source.volume1
dc.source.issue4
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/infdis_pp/13
dc.identifier.contextkey684324
html.description.abstract<p>We have generated, by ethylmethane sulfonate mutagenesis, loss-of-function mutants in the Drosophila homolog of the mammalian I-kappa B kinase (IKK) complex component IKK gamma (also called NEMO). Our data show that Drosophila IKK gamma is required for the Relish-dependent immune induction of the genes encoding antibacterial peptides and for resistance to infections by Escherichia coli. However, it is not required for the Toll-DIF-dependent antifungal host defense. The results indicate distinct control mechanisms of the Rel-like transactivators DIF and Relish in the Drosophila innate immune response and show that Drosophila Toll does not signal through a IKK gamma-dependent signaling complex. Thus, in contrast to the vertebrate inflammatory response, IKK gamma is required for the activation of only one immune signaling pathway in Drosophila.</p>
dc.identifier.submissionpathinfdis_pp/13
dc.contributor.departmentDepartment of Medicine, Division of Infectious Diseases and Immunology
dc.source.pages342-7


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