001     140635
005     20240321220839.0
024 7 _ |a 10.1038/s41418-018-0164-x
|2 doi
024 7 _ |a pmid:30026495
|2 pmid
024 7 _ |a pmc:PMC6462001
|2 pmc
024 7 _ |a 1350-9047
|2 ISSN
024 7 _ |a 1476-5403
|2 ISSN
024 7 _ |a altmetric:45225269
|2 altmetric
037 _ _ |a DZNE-2020-06957
041 _ _ |a English
082 _ _ |a 610
100 1 _ |a Aalto, Anna L
|b 0
245 _ _ |a M1-linked ubiquitination by LUBEL is required for inflammatory responses to oral infection in Drosophila.
260 _ _ |a London
|c 2019
|b Macmillan
264 _ 1 |3 online
|2 Crossref
|b Springer Science and Business Media LLC
|c 2018-07-19
264 _ 1 |3 print
|2 Crossref
|b Springer Science and Business Media LLC
|c 2019-05-01
336 7 _ |a article
|2 DRIVER
336 7 _ |a Output Types/Journal article
|2 DataCite
336 7 _ |a Journal Article
|b journal
|m journal
|0 PUB:(DE-HGF)16
|s 1588089481_27436
|2 PUB:(DE-HGF)
336 7 _ |a ARTICLE
|2 BibTeX
336 7 _ |a JOURNAL_ARTICLE
|2 ORCID
336 7 _ |a Journal Article
|0 0
|2 EndNote
520 _ _ |a Post-translational modifications such as ubiquitination play a key role in regulation of inflammatory nuclear factor-κB (NF-κB) signalling. The Drosophila IκB kinase γ (IKKγ) Kenny is a central regulator of the Drosophila Imd pathway responsible for activation of the NF-κB Relish. We found the Drosophila E3 ligase and HOIL-1L interacting protein (HOIP) orthologue linear ubiquitin E3 ligase (LUBEL) to catalyse formation of M1-linked linear ubiquitin (M1-Ub) chains in flies in a signal-dependent manner upon bacterial infection. Upon activation of the Imd pathway, LUBEL modifies Kenny with M1-Ub chains. Interestingly, the LUBEL-mediated M1-Ub chains seem to be targeted both directly to Kenny and to K63-linked ubiquitin chains conjugated to Kenny by DIAP2. This suggests that DIAP2 and LUBEL work together to promote Kenny-mediated activation of Relish. We found LUBEL-mediated M1-Ub chain formation to be required for flies to survive oral infection with Gram-negative bacteria, for activation of Relish-mediated expression of antimicrobial peptide genes and for pathogen clearance during oral infection. Interestingly, LUBEL is not required for mounting an immune response against systemic infection, as Relish-mediated antimicrobial peptide genes can be expressed in the absence of LUBEL during septic injury. Finally, transgenic induction of LUBEL-mediated M1-Ub drives expression of antimicrobial peptide genes and hyperplasia in the midgut in the absence of infection. This suggests that M1-Ub chains are important for Imd signalling and immune responses in the intestinal epithelia, and that enhanced M1-Ub chain formation is able to drive chronic intestinal inflammation in flies.
536 _ _ |a 341 - Molecular Signaling (POF3-341)
|0 G:(DE-HGF)POF3-341
|c POF3-341
|f POF III
|x 0
542 _ _ |i 2018-07-19
|2 Crossref
|u https://creativecommons.org/licenses/by/4.0
588 _ _ |a Dataset connected to CrossRef, PubMed,
650 _ 2 |a Animals
|2 MeSH
650 _ 2 |a Bacterial Infections: genetics
|2 MeSH
650 _ 2 |a Bacterial Infections: microbiology
|2 MeSH
650 _ 2 |a Disease Models, Animal
|2 MeSH
650 _ 2 |a Drosophila: genetics
|2 MeSH
650 _ 2 |a Drosophila Proteins: genetics
|2 MeSH
650 _ 2 |a Gram-Negative Bacteria: pathogenicity
|2 MeSH
650 _ 2 |a Humans
|2 MeSH
650 _ 2 |a Immunity, Innate: genetics
|2 MeSH
650 _ 2 |a Inflammation: genetics
|2 MeSH
650 _ 2 |a Inflammation: microbiology
|2 MeSH
650 _ 2 |a Inhibitor of Apoptosis Proteins: genetics
|2 MeSH
650 _ 2 |a Mouth: microbiology
|2 MeSH
650 _ 2 |a Mouth: pathology
|2 MeSH
650 _ 2 |a NF-kappa B: genetics
|2 MeSH
650 _ 2 |a Protein Processing, Post-Translational: genetics
|2 MeSH
650 _ 2 |a RNA-Binding Proteins: genetics
|2 MeSH
650 _ 2 |a Signal Transduction: genetics
|2 MeSH
650 _ 2 |a Transcription Factors: genetics
|2 MeSH
650 _ 2 |a Ubiquitin: genetics
|2 MeSH
650 _ 2 |a Ubiquitin-Protein Ligases: genetics
|2 MeSH
650 _ 2 |a Ubiquitination: genetics
|2 MeSH
700 1 _ |a Mohan, Aravind K
|b 1
700 1 _ |a Schwintzer, Lukas
|0 P:(DE-2719)2810987
|b 2
|u dzne
700 1 _ |a Kupka, Sebastian
|b 3
700 1 _ |a Kietz, Christa
|b 4
700 1 _ |a Walczak, Henning
|b 5
700 1 _ |a Broemer, Meike
|0 P:(DE-2719)2810307
|b 6
|u dzne
700 1 _ |a Meinander, Annika
|0 P:(DE-HGF)0
|b 7
|e Corresponding author
773 1 8 |a 10.1038/s41418-018-0164-x
|b : Springer Science and Business Media LLC, 2018-07-19
|n 5
|p 860-876
|3 journal-article
|2 Crossref
|t Cell Death & Differentiation
|v 26
|y 2018
|x 1350-9047
773 _ _ |a 10.1038/s41418-018-0164-x
|g Vol. 26, no. 5, p. 860 - 876
|0 PERI:(DE-600)1496681-5
|n 5
|q 26:5<860 - 876
|p 860-876
|t Cell death and differentiation
|v 26
|y 2018
|x 1350-9047
856 7 _ |2 Pubmed Central
|u http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6462001
909 C O |o oai:pub.dzne.de:140635
|p VDB
910 1 _ |a Deutsches Zentrum für Neurodegenerative Erkrankungen
|0 I:(DE-588)1065079516
|k DZNE
|b 2
|6 P:(DE-2719)2810987
910 1 _ |a Deutsches Zentrum für Neurodegenerative Erkrankungen
|0 I:(DE-588)1065079516
|k DZNE
|b 6
|6 P:(DE-2719)2810307
913 1 _ |a DE-HGF
|b Forschungsbereich Gesundheit
|l Erkrankungen des Nervensystems
|1 G:(DE-HGF)POF3-340
|0 G:(DE-HGF)POF3-341
|2 G:(DE-HGF)POF3-300
|v Molecular Signaling
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914 1 _ |y 2019
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LibraryCollectionCLSMajorCLSMinorLanguageAuthor
Marc 21