Anti-human STING antibody

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Monoclonal antibody against human STING (clone 3B5)

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2 x 100 µg


Monoclonal antibody against human STING for detection

Human STING detection with Anti-hSTING-IgG
Human STING detection with Anti-hSTING-IgG

Anti-hSTING-IgG (clone 3B5) is a monoclonal mouse IgG1 antibody against human STING (hSTING). This antibody was generated by InvivoGen using DNA immunization. It has been produced in hybridomas and purified by affinity chromatography.
Anti-hSTING-IgG has been selected for its ability to bind hSTING. It recognizes the most prevalent isoform “wild‑type” R232 and HAQ hSTING variants. This antibody can be used to detect hSTING using ELISA and Western blot.
STING (stimulator of interferon genes) is essential for the interferon response to cytoplasmic foreign or self-DNA. It directly senses cyclic dinucleotides (CDNs), which are important messengers in bacteria and innate immune agonists in mammals [1]. Several STING variants, that differ in their responses to CDNs, have been described in the human population [2].

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Key features:

  • Reacts with the “wild‑type” R232 (R71‑G230-R232-R293) hSTING variant
  • Reacts with the HAQ (H71‑A230-R232-Q293) hSTING variant
  • Provided azide-free
  • Each lot is functionally tested


  • Western blot


Read our review on STING



1. Sun L. et al., 2013. Cyclic GMP-AMP synthase is a cytosolic DNA sensor that activates the type I interferon pathway. Science. 339:786-91. 
2. Yi G. et al., 2013. Single nucleotide polymorphisms of human STING can affect innate immune response to cyclic dinucleotides. PLOS One. 8:e77846. 




Anti-hSTING-IgG recognition of recombinant hSTING. Recombinant hSTING was immobilized at 1 μg/mL (50 μL/well) in 96-well plate, followed by the addition of Anti-hSTING capture antibody and HRP-conjugated secondary antibody. Absorbance was read at 450 nm following addition of HRP substrate.

Western blot
Western blot

Detection of human STING by Western blot. Western blot analysis of lysates (40 μg) using Anti‑hSTING‑IgG (0.2 μg/ml), followed by HRP‑conjugated goat anti-mouse IgG1 secondary antibody (1:3000 dilution).
A: THP1‑Dual™ KO‑STING cells
B: THP1-Dual™ cells (endogenously expresses the HAQ hSTING variant)
C: 293T-Dual™ Null cells (does not express functional hSTING protein)
D: 293T-Dual™ hSTING-R232 cells (stably transfected with the R232 hSTING variant)

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Target: Human STING (hSTING) R232 variant (soluble CDN-binding domain)

Specificity: Reacts with the “wild‑type” R232 (R71‑G230-R232-R293) and HAQ (H71A230-R232-Q293) hSTING variants. This antibody reacts very poorly with murine STING. No reactivity was observed with the STING‑knockout cells.

Clonality: Monoclonal antibody

Clone: 3B5

Isotype: Mouse IgG1, kappa

Control: Mouse Control IgG1

Source: Hybridoma cells

Purity: Purified by affinity chromatography with protein G

Formulation: 0.2 µm filtered solution in a sodium phosphate buffer with glycine, saccharose, and stabilizing agents

Tested applications: Detection antibody for Western blot and ELISA.

Quality control:
   - The antibody has been validated by Western blot.
   - The absence of bacterial contamination (e.g. lipoproteins and endotoxins) has been confirmed using HEK-Blue™ TLR2 and HEK-Blue™ TLR4 cells.

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  • 2 x 100 µg of purified Anti-hSTING-IgG provided azide-free and lyophilized.

Product is shipped at room temperature.

Upon receipt, store lyophilized antibody at -20°C.

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STING (stimulator of interferon genes) has become a focal point in immunology research and drug discovery [1, 2]. In a healthy individual, STING functions as a signaling hub, orchestrating immune responses to pathogenic, tumoral, or self-DNA detected in the cytoplasm [2]. Upon activation, STING induces type I interferon (IFN) production through TANK-binding-kinase-I (TBK1)-mediated IFN regulatory factor (IRF3) signaling [2]. STING activation also leads to NF‑κBdependent inflammatory cytokine production [2]. In some autoimmune diseases such as STING-associated vasculopathy with onset in infancy (SAVI), STING is constitutively activated resulting in high IFN production [3, 4]. The discovery of a mechanism to pharmacologically inhibit STING should lead to new treatments for such diseases.



1. Haag S.M. et al., 2018. Targeting STING with covalent small-molecule inhibitors. Nature 559:269-73.
2. Ishikawa H. & Barber G.N. 2008. STING is an endoplasmic reticulum adaptor that facilitates innate immune signalling. Nature 455:674-8.
3. Liu Y. et al., 2014. Activated STING in a vascular and pulmonary syndrome. N Engl J Med. 371:507-18.
4. Jeremiah N. et al., 2013. Inherited STING-activating mutation underlies a familial inflammatory syndrome with lupus-like manifestations. J Clin Invest. 124:5516-20.

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