STING-Dependent Signaling
STING (stimulator of interferon genes) is a pattern recognition receptor and adapter protein that mediates an innate immune response following detection of cytoplasmic DNA. STING-dependent signaling is involved in certain autoimmune diseases and cancer immunology.
STING-Dependent Signaling Agonists |
|
|---|---|
| Cat. No. | 产品名称/活性 |
| 7706 | ADU-S100 disodium salt |
| STING agonist | |
| 5901 | c-Di-AMP sodium salt |
| Endogenous STING and DDX41 agonist; activates STING-dependent signaling | |
| 5900 | c-Di-GMP sodium salt |
| Endogenous STING and DDX41 agonist; activates STING-dependent signaling | |
| 5945 | 2',3'-cGAMP sodium salt |
| Endogenous high affinity STING agonist | |
| 6677 | CMA |
| Murine-selective STING agonist | |
| 5601 | DMXAA |
| mSTING agonist; induces antitumor immunological responses | |
| 7353 | MSA 2 |
| Non-nucleotide STING agonist; orally bioavailable | |
| 8120 | NVS-STG2 |
| STING agonist, molecular glue that causes oligomerization of STING | |
| 7741 | STING agonist C53 |
| Pan-polymorph STING agonist | |
STING-Dependent Signaling Antagonists |
|
| Cat. No. | 产品名称/活性 |
| 7040 | C 176 |
| mSTING antagonist | |
| 6675 | H 151 |
| STING antagonist | |
STING-Dependent Signaling Inhibitors |
|
| Cat. No. | 产品名称/活性 |
| 7820 | CU-76 |
| Selective inhibitor of cyclic GMP-AMP synthase (cGAS) | |
| 7904 | RU.521 |
| Potent and selective inhibitor of cyclic GMP-AMP synthase (cGAS) | |
Degraders |
|
| Cat. No. | 产品名称/活性 |
| 8053 | STING Degrader SP23 |
| Selective STING Degrader (PROTAC®) | |
Controls |
|
| Cat. No. | 产品名称/活性 |
| 8054 | STING Degrader N-Me-SP23 |
| Negative control for STING Degrader SP23 (Cat. No. 8053) | |
Other |
|
| Cat. No. | 产品名称/活性 |
| 7718 | 3',2'-cGAMP sodium salt |
| Induces expression of STING and STING-related genes; antiviral | |
| 1540 | DCPIB |
| Inhibits VRAC-mediated cGAMP transport | |
| 1370 | Sphingosine-1-phosphate |
| Activates VRAC-mediated cGAMP transport | |
STING (stimulator of interferon genes) is a pattern recognition receptor and adapter protein that is anchored in the endoplasmic reticulum (ER), and is highly expressed in immune cells. STING-dependent signaling mediates a toll-like receptor independent innate immune response following detection of cytoplasmic pathogens.
The invasion of a cell by a pathogen, such as a virus or bacterium, results in a host defence response mediated by the adapter protein STING. Foreign DNA is detected by cytosolic DNA sensors, which converge at STING to induce a signal transduction pathway, culminating in the production of proinflammatory cytokines and type 1 interferons (IFNs). STING is also activated by the bacteria secondary messenger cyclic dinucleotides (CDNs) c-di-GMP and c-di-AMP. Following detection of cytosolic DNA or CDNs, STING forms a dimer and translocates from the ER to perinuclear microsomes, where it is poly-ubiquitinated on K27 by the autophagy motility factor receptor (AMFR)-insulin-induced gene 1 (INSIG1) complex. Poly-ubiquitinated STING binds TBK1, and the STING-TBK1 complex activates the transcription factor interferon regulatory factor 3 (IRF3), which translocates into the nucleus to induce IFN gene expression.
STING is modulated by certain proteins, to ensure that the STING-dependent immune response is strong enough to eliminate invading pathogens, without being damaging to the host. The ubiquitin E3 ligases RNF5 and RNF26 promote STING proteasomal and autophagic degradation respectively, while the pattern recognition receptor NLRC3 prevents STING translocation from the ER to microsomes.
As well as having a role in innate immunity, STING has also been shown to be involved in autoimmune diseases and cancer immunology. STING has been shown to be activated by aberrant host DNA leaked from the nucleus, to induce a pro-inflammatory response. This mechanism may be of pathological importance for autoimmune diseases such as lupus erythematosus. STING-dependent signaling can also promote a T cell response against tumors, by detecting tumor-derived DNA. STING agonists administered into the tumors of mice, have been shown to induce an adaptive immune response resulting in tumor regression, thus providing a potential target for cancer immunotherapy.