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SUMMARY:A molecular mechanism of STING-mediated NF-κB activation
DTSTART:20250930T121500
DTSTAMP:20260531T071132Z
UID:454ea4a2fc3d5468149b8b441b2edf9d61d5f4b52376b6e3495096a9
CATEGORIES:Conferences - Seminars
DESCRIPTION:Rune Hartmann\, Department of Molecular Biology and Genetics\,
  Aarhus University\, Denmark\nThe stimulator of interferon genes (STING) p
 athway plays an important and conserved role in antiviral immunity. Human 
 STING (hSTING) has been shown to mediate antiviral immunity by activating 
 the transcription factors interferon regulatory factor 3 (IRF3) and nuclea
 r factor kappa-light-chain-enhancer of activated B cells (NF-κB). The act
 ivation of IRF3 by hSTING involves the C-terminal tail (CTT) of hSTING and
  TANK-binding kinase 1 (TBK1)\, and this process is well-described. In con
 trast\, the molecular mechanisms underlying NF-κB activation remain uncle
 ar. To elucidate this mechanism\, we exploited the conserved Drosophila me
 lanogaster STING (dSTING) pathway to uncover these mechanisms. Similar to 
 the human pathway\, dSTING confers antiviral immunity. However\, dSTING la
 cks the CTT and drives the expression of antiviral genes via the NF-κB ho
 molog Relish. Interestingly\, there are features of dSTING and hSTING medi
 ated NF-κB signaling which are conserved throughout evolution of animals.
  To elucidate how STING activate NF-κB signaling\, we have developed a pr
 oximity labeling approach that enables the specific detection of activity-
 dependent STING interactors. We demonstrate that IKKγ is recruited by STI
 NG upon activation and that the recruitment of IKKγ is essential for STIN
 G-mediate d activation of Relish. Moreover\, studies both in D. melanogast
 er and human cells indicate the pivotal role of linear ubiquitination in t
 he interaction between IKKγ and STING. Our findings suggest an evolutiona
 rily conserved mechanism of STING-mediated NF-κB activation. 
LOCATION:SV 1717 https://plan.epfl.ch/?room==SV%201717
STATUS:CONFIRMED
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