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STING Innate Immunity Signalling from the Golgi.

Tomohiko Taguchi1

  • 1Graduate School of Life Sciences, Tohoku University, Sendai, Japan. tomohiko.taguchi.b8@tohoku.ac.jp.

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The cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) pathway drives inflammation. STING activation involves ER-to-Golgi transport, with dysregulation linked to COPA syndrome.

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CholesterolIRF3Innate immune signallingProtein palmitoylationSTINGTBK1The trans-Golgi network

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Area of Science:

  • Immunology
  • Cell Biology
  • Molecular Biology

Background:

  • The cGAS-STING pathway is a key regulator of innate immunity, sensing cytosolic double-stranded DNA (dsDNA) to initiate inflammatory responses.
  • Activation involves STING translocation from the endoplasmic reticulum (ER) to the Golgi apparatus, leading to type I interferon production via TBK1 and IRF3.
  • Dysregulated membrane trafficking between the ER and Golgi is implicated in autoinflammatory diseases like COPA syndrome.

Purpose of the Study:

  • To explore the regulation of cGAS-STING pathway activation by membrane trafficking dynamics.
  • To elucidate the molecular mechanisms governing TBK1/IRF3 activation at the trans-Golgi network (TGN).

Main Methods:

  • Investigating STING localization and dynamics using live-cell imaging.
  • Analyzing protein-protein interactions at the TGN.
  • Utilizing genetic models of COPA syndrome to study ER-Golgi transport defects.

Main Results:

  • STING translocation from the ER to the Golgi is essential for its activation.
  • Specific membrane trafficking events at the TGN are crucial for TBK1/IRF3 recruitment and activation.
  • Mutations affecting ER-Golgi transport disrupt STING signaling and contribute to autoinflammation.

Conclusions:

  • Membrane traffic between the ER and Golgi is a critical regulatory checkpoint for the cGAS-STING pathway.
  • Targeting STING-mediated signaling and associated membrane trafficking pathways holds therapeutic potential for inflammatory diseases and cancer.