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Central Regulatory Role for SIN1 in Interferon γ (IFNγ) Signaling and Generation of Biological Responses

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dc.abstract.enThe precise signaling mechanisms by which type II IFN receptors control expression of unique genes to induce biological responses remain to be established. We provide evidence that Sin1, a known element of the mammalian target of rapamycin complex 2 (mTORC2), is required for IFNγ-induced phosphorylation and activation of AKT and that such activation mediates downstream regulation of mTORC1 and its effectors. These events play important roles in the assembly of the eukaryotic translation initiation factor 4F (eIF4F) and mRNA translation of IFN-stimulated genes. Interestingly, IFNγ-induced tyrosine phosphorylation of STAT1 is reduced in cells with targeted disruption of Sin1, leading to decreased transcription of several IFNγ-inducible genes in an mTORC2-independent manner. Additionally, our studies establish that Sin1 is essential for generation of type II IFN-dependent antiviral effects and antiproliferative responses in normal and malignant hematopoiesis. Together, our findings establish an important role for Sin1 in both transcription and translation of IFN-stimulated genes and type II IFN-mediated biological responses, involving both mTORC2-dependent and -independent functions.
dc.affiliationUniwersytet Warszawski
dc.contributor.authorJemielity, Jacek
dc.date.accessioned2024-01-24T19:05:07Z
dc.date.available2024-01-24T19:05:07Z
dc.date.issued2017
dc.description.financeNie dotyczy
dc.description.number11
dc.description.volume292
dc.identifier.doi10.1074/JBC.M116.757666
dc.identifier.issn0021-9258
dc.identifier.urihttps://repozytorium.uw.edu.pl//handle/item/102805
dc.identifier.weblinkhttp://www.jbc.org/content/292/11/4743.abstract
dc.languageeng
dc.pbn.affiliationchemical sciences
dc.relation.ispartofJournal of Biological Chemistry
dc.relation.pages4743-4752
dc.rightsClosedAccess
dc.sciencecloudnosend
dc.titleCentral Regulatory Role for SIN1 in Interferon γ (IFNγ) Signaling and Generation of Biological Responses
dc.typeJournalArticle
dspace.entity.typePublication