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摘要
En 中文
Two studies published in this issue of JEM, by Lepelley et al. (https://doi.org/10.1084/jem.20200600) and Deng et al. (https:// doi.org/10.1084/jem.20201045), and two additional manuscripts by Mukai et al. (https://doi.org/10.1101/2020.05.20. 107664 Preprint v1) and Steiner et al. (https://doi.org/10.1101/2020.07.09.194399 Preprint v1) demonstrate that COPA syndrome-associated high interferon titers are linked to mutations in COPA preventing STING's retrieval from the Golgi back to the ER and thereby causing chronic immune activation.
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期刊
J
IF:
10.6
论文数:
2.4W
被引数:
6.8W
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引用论文
The Ca2+ sensor STIM1 regulates the type I interferon response by retaining the signaling adaptor STING at the endoplasmic reticulumCa2传感器STIM1通过在内质网上保留信号接头来调节I型干扰素反应.png)
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OAAI
NATURE IMMUNOLOGYIF27.6
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收藏A defect in COPI-mediated transport of STING causes immune dysregulation in COPA syndromeCop1介导的STING运输缺陷导致COPA综合征的免疫失调OAAI
OAAI分享收藏STEEP mediates STING ER exit and activation of signalingSTEEP介导STING ER退出和信号激活NATURE IMMUNOLOGYOAAI
NATURE IMMUNOLOGYIF27.6
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