- Euarchontoglires; Primates; Haplorrhini; Catarrhini; Hominidae; Homo
- Also known as
- ERIS; MITA; MPYS; SAVI; NET23; STING; hMITA; hSTING; STING-beta
- Summary
- This gene encodes a five transmembrane protein that functions as a major regulator of the innate immune response to viral and bacterial infections. The encoded protein is a pattern recognition receptor that detects cytosolic nucleic acids and transmits signals that activate type I interferon responses. The encoded protein has also been shown to play a role in apoptotic signaling by associating with type II major histocompatibility complex. Mutations in this gene are the cause of infantile-onset STING-associated vasculopathy. Alternate splicing results in multiple transcript variants. [provided by RefSeq, Sep 2014]
- Expression
- Ubiquitous expression in lung (RPKM 37.4), spleen (RPKM 28.8) and 24 other tissues
STING-mediated type-I interferons contribute to the neuroinflammatory process and detrimental effects following traumatic brain injury. Abdullah A, et al. J Neuroinflammation, 2018 Nov 21.
PMID 30463579, Free PMC Article
Extracellular Vesicles Released by Herpes Simplex Virus 1-Infected Cells Block Virus Replication in Recipient Cells in a STING-Dependent Manner. Deschamps T, et al. J Virol, 2018 Sep 15. PMID 29976662,
Emerging Alphaviruses Are Sensitive to Cellular States Induced by a Novel Small-Molecule Agonist of the STING Pathway. Gall B, et al. J Virol, 2018 Mar 15. PMID 29263267,
Free PMC Article
STING signalling: an emerging common pathway in autoimmunity and cancer.
McCaffary D. Immunopharmacol Immunotoxicol, 2017 Oct. PMID 28724326
Activation of Stimulator of Interferon Genes in Hepatocytes Suppresses the Replication of Hepatitis B Virus. Guo F, et al. Antimicrob Agents Chemother, 2017 Oct. PMID 28717041,
Free PMC Article
See all (152) citations in PubMed GeneRIFs:
Gene References Into FunctionsWhat's a GeneRIF?
this study demonstrated that the Increased levels of STING are detected following traumatic brain injury.
Here, we report that the ubiquitin-binding selective autophagy receptor p62/SQSTM1 is essential for DNA- and cGAMP-stimulated degradation of STING.
We present physiological evidence that UBXN3B positively regulates stimulator-of-interferon genes (STING) signaling.
Mechanistic studies demonstrate that UBXN3B interacts with both STING and its E3 ligase TRIM56, and facilitates STING ubiquitination, dimerization, trafficking, and consequent recruitment and phosphorylation of TBK1.
STAG2 deficiency induces interferon responses via cGAS-STING pathway and restricts virus infection.
STING-IRF3 pathway promotes hepatocyte injury and dysfunction by inducing inflammation and apoptosis and by disturbing glucose and lipid metabolism.
Data show that both cyclic GMP-AMP synthase (cGAS) and interferon-gamma inducible protein 16 (IFI16) are required for the activation of membrane protein STING (STING) and an innate immune response to exogenous DNA and DNA viruses.
PUMA promotes the cytosolic release of mitochondrial DNA and activation of the DNA sensors DAI/Zbp1 and STING, leading to enhanced RIP3 and MLKL phosphorylation in a positive feedback loop.
identified nitro-fatty acids as endogenously formed inhibitors of STING signaling and propose for these lipids to be considered in the treatment of STING-dependent inflammatory diseases.
Cells of human individuals carrying HAQ TMEM173, which encodes a common hypomorphic variant of STING, were largely or partly defective in inducing type I IFNs and proinflammatory cytokines upon infection.
Our studies indicate that the (extracellular vesicles) EVs released by HSV-1-infected cells carry innate immune components such as STING and other host and viral factors; they can activate innate immune responses in recipient cells and inhibit HSV-1 replication.
The implication of these data is that the EVs released by HSV-1-infected cells could control HSV-1 dissemination promoting its persistence in the host.
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