The STING1 network regulates autophagy and cell death

被引:147
|
作者
Zhang, Ruoxi [1 ]
Kang, Rui [1 ]
Tang, Daolin [1 ]
机构
[1] UT Southwestern Med Ctr, Dept Surg, Dallas, TX 75390 USA
关键词
ENDOPLASMIC-RETICULUM STRESS; INNATE IMMUNE SENSOR; GMP-AMP SYNTHASE; DNA SENSOR; INDUCE AUTOPHAGY; TUBERCULOSIS DNA; BYSTANDER CELLS; I INTERFERONS; MYELOID CELLS; CYTOSOLIC DNA;
D O I
10.1038/s41392-021-00613-4
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Cell death and immune response are at the core of life. In past decades, the endoplasmic reticulum (ER) protein STING1 (also known as STING or TMEM173) was found to play a fundamental role in the production of type I interferons (IFNs) and pro-inflammatory cytokines in response to DNA derived from invading microbial pathogens or damaged hosts by activating multiple transcription factors. In addition to this well-known function in infection, inflammation, and immunity, emerging evidence suggests that the STING1-dependent signaling network is implicated in health and disease by regulating autophagic degradation or various cell death modalities (e.g., apoptosis, necroptosis, pyroptosis, ferroptosis, mitotic cell death, and immunogenic cell death [ICD]). Here, we outline the latest advances in our understanding of the regulating mechanisms and signaling pathways of STING1 in autophagy and cell death, which may shed light on new targets for therapeutic interventions.
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页数:13
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