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STEEP mediates STING ER exit and activation of signaling

Authors
  • Zhang, Bao-cun1
  • Nandakumar, Ramya1
  • Reinert, Line S.1
  • Huang, Jinrong1, 2
  • Laustsen, Anders1
  • Gao, Zong-liang1
  • Sun, Cheng-long1
  • Jensen, Søren Beck1
  • Troldborg, Anne1, 1, 3
  • Assil, Sonia1
  • Berthelsen, Martin F.1, 1
  • Scavenius, Carsten1
  • Zhang, Yan1
  • Windross, Samuel J.1
  • Olagnier, David1
  • Prabakaran, Thaneas1
  • Bodda, Chiranjeevi1
  • Narita, Ryo1, 1
  • Cai, Yujia1
  • Zhang, Cong-gang4, 5
  • And 11 more
  • 1 Aarhus University, Aarhus, Denmark , Aarhus (Denmark)
  • 2 University of Copenhagen, Copenhagen, Denmark , Copenhagen (Denmark)
  • 3 Aarhus University Hospital, Aarhus, Denmark , Aarhus (Denmark)
  • 4 University of Texas Southwestern Medical Center, Dallas, TX, USA , Dallas (United States)
  • 5 Howard Hughes Medical Institute, University of Texas Southwestern Medical Center, Dallas, TX, USA , Dallas (United States)
  • 6 Institute for Cancer Research, Oslo University Hospital, Oslo, Norway , Oslo (Norway)
  • 7 INSERM, CNRS, Université de Montpellier, Montpellier, France , Montpellier (France)
  • 8 Osaka University, Osaka, Japan , Osaka (Japan)
  • 9 National Institute of Allergy and Infectious Diseases (NIAID), National Institutes of Health (NIH), Bethesda, MD, USA , Bethesda (United States)
  • 10 Aarhus Institute of Advanced Studies (AIAS), Aarhus University, Aarhus, Denmark , Aarhus (Denmark)
Type
Published Article
Journal
Nature Immunology
Publisher
Springer Nature
Publication Date
Jul 20, 2020
Volume
21
Issue
8
Pages
868–879
Identifiers
DOI: 10.1038/s41590-020-0730-5
Source
Springer Nature
License
Yellow

Abstract

STING ER exit is the rate-limiting step in STING signaling, but the mechanism that drives this process is not understood. Paludan and colleagues identify CxORF56, called STEEP here, as a positive regulator of STING signaling.

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