The SEL1L–HRD1 endoplasmic reticulum-associated degradation pathway negatively regulates STING-mediated innate immunity by ubiquitinating and targeting STING for proteasomal degradation, thereby limiting its activation.
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References
Guerriero, C. J. & Brodsky, J. L. The delicate balance between secreted protein folding and endoplasmic reticulum-associated degradation in human physiology. Physiol. Rev. 92, 537–576 (2012). A review article on ERAD.
Sun, S. et al. IRE1α is an endogenous substrate of endoplasmic-reticulum-associated degradation. Nat. Cell Biol. 17, 1546–1555 (2015). This paper reports that SEL1L–HRD1 ERAD degrades the unfolded protein response sensor IRE1.
Ji, Y. et al. The Sel1L–Hrd1 endoplasmic reticulum-associated degradation complex manages a key checkpoint in B cell development. Cell Rep. 16, 2630–2640 (2016). This paper reports a critical role of SEL1L–HRD1 ERAD in developing B cells by regulating the abundance of pre-B cell receptor protein at the ER.
Bhattacharya, A. & Qi, L. ER-associated degradation in health and disease — from substrate to organism. J. Cell Sci. 132, jcs232850 (2019). A review article on the physiological importance of SEL1L–HRD1 ERAD and its endogenous substrates.
Ishikawa, H. & Barber, G. N. STING is an endoplasmic reticulum adaptor that facilitates innate immune signalling. Nature 455, 674–678 (2008). This paper reports the cloning and ER localization of STING.
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This is a summary of: Ji, Y. et al. SEL1L–HRD1 endoplasmic reticulum-associated degradation controls STING-mediated innate immunity by limiting the size of the activable STING pool. Nat. Cell Biol. https://doi.org/10.1038/s41556-023-01138-4 (2023).
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Endoplasmic reticulum-associated degradation shown to regulate innate immunity. Nat Cell Biol 25, 641–642 (2023). https://doi.org/10.1038/s41556-023-01139-3
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DOI: https://doi.org/10.1038/s41556-023-01139-3
