Active • Host: E. coli • AA: 138-379 • Tag: N-terminal His • MW: 28.8 kDa
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STING R232 variant (human, recombinant)

Item No. 22816

Product Insert (PDF)Safety Data Sheet (SDS) (PDF)
Technical Information
Synonyms
  • Endoplasmic Reticulum Interferon Stimulator
  • ERIS
  • Mediator of IRG3 Activation
  • MITA
  • Mitochondrial Mediator of IRF3 Activation
  • MPYS
  • Stimulator of Interferon Genes
  • Stimulator of Interferon Response cGAMP Interactor 1
  • STING1
  • N-Terminal Methionine-Proline-Tyrpsine-Serine Plasma Membrane Tetraspanner
  • TMEM173
  • Transmembrane Protein 173
Purity
≥80% estimated by SDS-PAGE
Source
Recombinant N-terminal His-tagged STING catalytic domain purified from E. coli
Amino Acids
138-379 (N-terminal truncation), R232 variant
Formulation (Request formulation change)
50 mM HEPES, pH 8.0, 150 mM sodium chloride, 10% glycerol
UniProt Accession №
Q86WV6
Shipping & Storage Information
Storage
-80°C
Shipping
Dry ice in continental US; may vary elsewhere
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    100 µg

    $649

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    Product Description

    Stimulator of interferon genes (STING) is a component of the innate immune response that binds to cyclic dinucleotides, which are bacterial second messengers, leading to activation of NF-κB and transcription of immunomodulatory genes, including type I interferon (IFN).1,2,3,4 The R232 variant is the most common variant in the human population, found at a frequency of 57.9% in the 1000 Genome Project.5 The SNP variant H232 (Item No. 22815) is found at a 13.7% frequency. Various mutations in STING either reduce or increase its activity. Gain-of-function mutations in STING, including R284M (Item No. 23594) and V155M, lead to constitutive activation and enhancement of the type I IFN response.5,6 The V155M mutation is associated with a systemic inflammatory condition, including pulmonary fibrosis and autoimmune factors.6 Mutations that reduce STING activity include K224R (Item No. 23593), which reduces ubiquitination of STING thereby disrupting its localization within the cell, and the double mutation G230A, R293Q (Item No. 23592), which reduces the IFN response.5,7 A T596A mutation present in the mouse strain Goldenticket leads to a complete loss of STING protein and lack of a type I IFN response to infection by Listeria.8

    WARNING This product is not for human or veterinary use.

    References & Product Citations
    Product Description References

    1. Burdette, D.L., Monroe, K.M., Sotelo-Troha, K., et al. STING is a direct innate immune sensor of cyclic-di-GMP. Nature 478(7370), 515-518 (2011).

    2. Sun, L., Wu, J., Du, F., et al. Cyclic GMP-AMP synthase is a cytosolic DNA sensor that activates the type I interferon pathway. Science 339(6121), 786-791 (2013).

    3. Wu, J., Sun, L., Chen, X., et al. Cyclic GMP-AMP is an endogenous second messenger in innate immune signaling by cytosolic DNA. Science 339(6121), 826-830 (2013).

    4. Konno, H., Konno, K., and Barber, G.N. Cyclic dinucleotides trigger ULK1 (ATG1) phosphorylation of STING to prevent sustained innate immune signaling. Cell 155(3), 688-698 (2013).

    5. Yi, G., Brendel, V.P., Shu, C., et al. Single nucleotide polymorphisms of human STING can affect innate immune response to cyclic dinucleotides. PLoS One 8(10), e77846 (2013).

    6. Jeremiah, N., Neven, B., Gentili, M., et al. Inherited STING-activating mutation underlies a familial inflammatory syndrome with lupus-like manifestations. J. Clin. Invest. 124(12), 5516-5520 (2014).

    7. Ni, G., Konno, H., and Barber, G.N. Ubiquitination of STING at lysine 224 controls IRF3 activation. Sci. Immunol. 2(11), eaah7119 (2017).

    8. Sauer, J.D., Sotelo-Troha, K., von Moltke, J., et al. The N-ethyl-N-nitrosourea-induced Goldenticket mouse mutant reveals an essential function of Sting in the in vivo interferon response to Listeria monocytogenes and cyclic dinucleotides. Infect. Immun. 79(2), 688-694 (2011).