STING-N200

Expression-ready ORF Clones

Human STING gene, I200N variant

STING (stimulator of interferon genes; also known as TMEM173, MITA, MPYS, and ERIS) is essential for the interferon (IFN) response to microbial or self-DNA, and acts as a direct sensor of cyclic dinucleotides (CDNs). Genetic variation in STING can affect CDN recognition and downstream signaling.

The human STING-N200 variant harbors an I200N missense substitution, corresponding to the I199N mutation found in the Goldenticket (Gt) mouse. Residue I200 is buried within the STING protomer, and substitution of this conserved residue disrupts STING function. The I200N variant exhibits impaired CDN-induced signaling and loss of type I IFN responses, consistent with a functionally null STING phenotype [1,2]. The corresponding I199N mutation in the Gt mouse results in loss of detectable STING protein and impaired type I IFN responses to bacterial CDNs and Listeria monocytogenes [2].

References:

1. Yin Q. et al., 2012. Cyclic di-GMP sensing via the innate immune signaling protein STING. Mol Cell 46(6):735-45.
2. Sauer JD. et al., 2011. 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):688-94.