In Stock Cell Lines
Sting1 Knockout RCS Cell Line is a CRISPR/Cas9-edited knockout cell line derived from rat chondrosarcoma-derived chondrocyte-like RCS cells. This model eliminates STING1 (TMEM173), a critical adaptor protein in the cGAS-STING pathway that mediates innate immune responses to cytosolic DNA. STING1 activation leads to downstream signaling through TBK1 and IRF3/NF-??B, inducing type I interferons and pro-inflammatory cytokines such as IFN-??, IL-6, and TNF-??. Within chondrocytes, STING1 drives inflammation and cartilage degradation, making this knockout ideal for studying osteoarthritis mechanisms, autoinflammatory signaling, and DNA sensing pathways. Application areas include drug screening for STING1 inhibitors, analysis of inflammatory gene expression, and dissection of cartilage matrix homeostasis. Typical assays involve Western blot, RT-qPCR, ELISA, and immunofluorescence.
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The Sting1 Knockout RCS Cell Line is a CRISPR/Cas9-edited knockout cell line featuring targeted disruption of the Sting1 gene in the RCS chondrocyte-like cell background. This product eliminates expression of STING1 (also known as TMEM173), an endoplasmic reticulum-resident adaptor protein central to innate immune sensing of cytosolic DNA. The knockout line provides a clean loss-of-function model for investigating STING1-dependent signaling cascades without confounding pathway interference.
The parental RCS cell line originates from a rat chondrosarcoma and retains a chondrocytic phenotype, characterized by robust expression of cartilage matrix molecules including aggrecan and type II collagen. Because RCS cells faithfully recapitulate many aspects of chondrocyte biology and matrix metabolism, they are a widely accepted in vitro system for cartilage research, particularly in studies of chondrocyte differentiation, matrix synthesis, and degenerative disease mechanisms.
STING1 functions as a direct sensor of cyclic dinucleotides such as 2’3′-cGAMP generated by the DNA receptor cGAS upon encountering cytosolic DNA from mitochondria, viral sources, or other triggers. Ligand engagement promotes STING1 homodimerization and translocation from the endoplasmic reticulum to the Golgi, where it scaffolds the kinases TBK1 and IKK. These kinases phosphorylate and activate the transcription factors IRF3 and NF-??B, respectively. Activated IRF3 and NF-??B drive transcription of type I interferons (including IFN-??) and pro-inflammatory cytokines like IL-6 and TNF-??. STING1 also interacts with auxiliary DNA sensors such as IFI16 and DDX41 and functions upstream of TBK1-mediated IRF3 signaling. Overall, STING1 is a key node connecting cytosolic DNA detection to broad innate immune transcriptional programs.
In chondrocytes, STING1-mediated signaling contributes to the inflammatory milieu associated with cartilage breakdown in osteoarthritis and inflammatory arthritis. Upon activation, STING1 triggers NF-??B-dependent induction of matrix-degrading enzymes and cytokines, compromising cartilage matrix integrity. The Sting1 Knockout RCS Cell Line thus enables direct examination of STING1??s role in chondrocyte-driven inflammation and matrix homeostasis, separating these effects from other innate immune pathways.
This knockout model supports a range of mechanistic and drug discovery studies, including dissection of the cGAS-STING-TBK1-IRF3/NF-??B axis, screening for STING1 pathway inhibitors, and evaluating anti-inflammatory compounds in a chondrocyte context. Researchers can employ Western blot detection of STING1, phosphorylated TBK1, and phosphorylated IRF3; RT-qPCR profiling of IFN-??, IL-6, and MMP13; ELISA for cytokine secretion; immunofluorescence for STING1 subcellular localization; and Alcian blue staining for cartilage matrix. The line is also useful for DNA damage and apoptosis assays. For further details, contact Ascent Research.
