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IL-17 undermines lo...
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Lu, QiongxuanUmeå universitet,Umeå centrum för molekylär medicin (UCMM),Wallenberg centrum för molekylär medicin vid Umeå universitet (WCMM),Umeå Centre for Microbial Research (UCMR),Changchun Chen
(author)
IL-17 undermines longevity and stress tolerance by inhibiting a protective transcriptional network
Publisher, publication year, extent ...
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Cold Spring Harbor Laboratory,2024
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printrdacarrier
Numbers
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LIBRIS-ID:oai:DiVA.org:umu-208124
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https://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-208124URI
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https://doi.org/10.1101/2023.01.13.523898DOI
Supplementary language notes
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Language:English
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Summary in:English
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Subject category:vet swepub-contenttype
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Subject category:ovr swepub-publicationtype
Notes
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Aberrant cytokine secretion contributes to the pathogenesis of autoimmune diseases and age-related disorders, but the molecular mechanism underlying this is not entirely clear. Here, we elucidate how interleukin-17 (IL-17) overactivation shortens lifespan and damages defense mechanisms against stress inC. elegans. Our analysis reveals that NHR-49, theC. elegansortholog of human PPARα and HNF4, is the central component in the transcriptional network undermined by increased IL-17 signaling. Both NHR-49 and its coactivator MDT-15 physically interact with the downstream components of IL-17 pathway, and their expression is significantly decreased when IL-17 signaling is enhanced. IL-17 overactivation also induces the expression and nucleus entry of theC. elegansortholog of NF-κB inhibitor NFKI-1/IκBζ to repress the activity of transcriptional coactivator MDT-15 and CBP-1. IL-17 signaling acts on neurons to modulate the activity of NFKI-1/IκBζ and NHR-49. In addition, persistent IL-17 activation decreases the expression of HLH-30/TFEB, leading to the reduced transcription of lysosomal lipase genes in the distal tissues. All these jointly contribute to the increased sensitivity to oxidative stress of animals with enhanced IL-17 signaling. Collectively, our work illustrates a transcription system undermined by IL-17 overactivation in the animals without NF-κB, and provides mechanistic insight into the pathogenesis of abnormal IL-17 secretion.
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Vladareanu, IoanaUmeå universitet,Umeå centrum för molekylär medicin (UCMM),Wallenberg centrum för molekylär medicin vid Umeå universitet (WCMM),Umeå Centre for Microbial Research (UCMR)(Swepub:umu)iovl0001
(author)
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Zhao, Lina,1990-Umeå universitet,Umeå centrum för molekylär medicin (UCMM),Wallenberg centrum för molekylär medicin vid Umeå universitet (WCMM),Umeå Centre for Microbial Research (UCMR),Changchun Chen(Swepub:umu)lizh0020
(author)
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Nilsson, LarsUmeå universitet,Umeå centrum för molekylär medicin (UCMM),Wallenberg centrum för molekylär medicin vid Umeå universitet (WCMM),Umeå Centre for Microbial Research (UCMR)(Swepub:umu)lani0001
(author)
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Henriksson, JohanUmeå universitet,Institutionen för molekylärbiologi (Medicinska fakulteten),Molekylär Infektionsmedicin, Sverige (MIMS),Umeå Centre for Microbial Research (UCMR)(Swepub:umu)johe6219
(author)
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Chen, ChangchunUmeå universitet,Umeå centrum för molekylär medicin (UCMM),Wallenberg centrum för molekylär medicin vid Umeå universitet (WCMM),Umeå Centre for Microbial Research (UCMR)(Swepub:umu)chch0005
(author)
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Umeå universitetUmeå centrum för molekylär medicin (UCMM)
(creator_code:org_t)
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