Reduced insulin/IGF1 signaling prevents immune aging via ZIP-10/bZIP-mediated feedforward loop

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dc.contributor.authorLee, Yujinko
dc.contributor.authorJung, Yoonjiko
dc.contributor.authorJeong, Dae-Eunko
dc.contributor.authorHwang, Wooseonko
dc.contributor.authorHam, Seokjinko
dc.contributor.author박혜은ko
dc.contributor.authorKwon, Sujeongko
dc.contributor.authorAshraf, Jasmine M.ko
dc.contributor.authorMurphy, Coleen T.ko
dc.contributor.authorLee, Seung-Jae, Vko
dc.date.accessioned2021-03-30T01:50:22Z-
dc.date.available2021-03-30T01:50:22Z-
dc.date.created2021-03-30-
dc.date.created2021-03-30-
dc.date.issued2021-03-
dc.identifier.citationJOURNAL OF CELL BIOLOGY, v.220, no.5-
dc.identifier.issn0021-9525-
dc.identifier.urihttp://hdl.handle.net/10203/282189-
dc.description.abstractA hallmark of aging is immunosenescence, a decline in immune functions, which appeared to be inevitable in living organisms, including Caenorhabditis elegans. Here, we show that genetic inhibition of the DAF-2/insulin/IGF-1 receptor drastically enhances immunocompetence in old age in C. elegans. We demonstrate that longevity-promoting DAF-16/FOXO and heat-shock transcription factor 1 (HSF-1) increase immunocompetence in old daf-2(-) animals. In contrast, p38 mitogen-activated protein kinase 1 (PMK-1), a key determinant of immunity, is only partially required for this rejuvenated immunity. The up-regulation of DAF-16/FOXO and HSF-1 decreases the expression of the zip-10/bZIP transcription factor, which in turn down-regulates INS7, an agonistic insulin-like peptide, resulting in further reduction of insulin/IGF-1 signaling (IIS). Thus, reduced IIS prevents immune aging via the up-regulation of anti-aging transcription factors that modulate an endocrine insulin-like peptide through a feedforward mechanism. Because many functions of 115 are conserved across phyla, our study may lead to the development of strategies against immune aging in humans.-
dc.languageEnglish-
dc.publisherROCKEFELLER UNIV PRESS-
dc.titleReduced insulin/IGF1 signaling prevents immune aging via ZIP-10/bZIP-mediated feedforward loop-
dc.typeArticle-
dc.identifier.wosid000626391900001-
dc.identifier.scopusid2-s2.0-85102705308-
dc.type.rimsART-
dc.citation.volume220-
dc.citation.issue5-
dc.citation.publicationnameJOURNAL OF CELL BIOLOGY-
dc.identifier.doi10.1083/jcb.202006174-
dc.contributor.localauthorLee, Seung-Jae, V-
dc.contributor.nonIdAuthorLee, Yujin-
dc.contributor.nonIdAuthorJeong, Dae-Eun-
dc.contributor.nonIdAuthorHwang, Wooseon-
dc.contributor.nonIdAuthorHam, Seokjin-
dc.contributor.nonIdAuthorAshraf, Jasmine M.-
dc.contributor.nonIdAuthorMurphy, Coleen T.-
dc.description.isOpenAccessN-
dc.type.journalArticleArticle-
dc.subject.keywordPlusCAENORHABDITIS-ELEGANS-
dc.subject.keywordPlusLIFE-SPAN-
dc.subject.keywordPlusTRANSCRIPTION FACTOR-
dc.subject.keywordPlusDEPENDENT REGULATION-
dc.subject.keywordPlusGENE-EXPRESSION-
dc.subject.keywordPlusINNATE IMMUNITY-
dc.subject.keywordPlusDAUER FORMATION-
dc.subject.keywordPlusLONGEVITY-
dc.subject.keywordPlusDAF-2-
dc.subject.keywordPlusRESISTANCE-
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