In Stock Cell Lines
Mus musculus (Mouse)
Brain
Adherent and suspension
The Sting1 Knockout BV-2 Cell Line is a CRISPR/Cas9-edited murine microglial cell line with targeted disruption of the Sting1 gene, abolishing expression of the STING adaptor protein. By eliminating cGAS-STING signaling, this model blocks TBK1-mediated phosphorylation of IRF3 and NF-??B, preventing induction of type I interferons (e.g., IFNB) and pro-inflammatory cytokines such as CXCL10. It is suitable for dissecting STING-dependent microglial responses in neuroinflammation, antiviral immunity, and cancer immunotherapy. Key applications include Western blotting, RT-qPCR, ELISA, and functional assays for phagocytosis and activation. Contact Ascent Research for more information.
BZW2 Knockout K562 Polyclonal Cells
Cat. No. ARG20347
MID1IP1 Knockout NCI-H1975 Polyclonal Cells
Cat. No. ARG16602
AP4B1 Knockout A2780 Polyclonal Cells
Cat. No. ARG28726
HNRNPAB Knockout HGC-27 Polyclonal Cells
Cat. No. ARG29952
NCOA7 Knockout MES-OV Polyclonal Cells
Cat. No. ARG6569
MAP4 Knockout Raji Polyclonal Cells
Cat. No. ARG2008
The Sting1 Knockout BV-2 Cell Line is a CRISPR/Cas9-edited knockout cell line derived from the BV-2 murine microglial cell line. This model features targeted disruption of the Sting1 gene, producing a loss of STING adaptor protein expression. It offers a stable, ready-to-use system for investigating cytosolic DNA-sensing pathways in microglial cells without the need for transient gene silencing.
BV-2 cells are an immortalized microglial cell line from C57BL/6 mice, extensively used to study central nervous system (CNS) immune surveillance and inflammatory responses. These cells retain key microglial functions, including phagocytosis and cytokine production, making them an ideal host for modeling neuroimmune signaling.
STING is an endoplasmic reticulum-resident homodimeric adaptor protein that, upon binding to the cyclic dinucleotide cGAMP produced by cGAS, oligomerizes and translocates to the Golgi apparatus. There, it recruits TANK-binding kinase 1 (TBK1), which phosphorylates STING itself and the transcription factors interferon regulatory factor 3 (IRF3) and nuclear factor-??B (NF-??B). Phosphorylated IRF3 dimerizes and translocates to the nucleus to drive transcription of type I interferons (e.g., IFNB) and interferon-stimulated genes, while NF-??B activates expression of pro-inflammatory cytokines and chemokines, including CCL5 and CXCL10. Additionally, STING interacts with autophagy regulators such as ATG9A and ULK1, linking DNA sensing to autophagic pathways. Knockout of Sting1 eliminates these signaling cascades, severely impairing innate immune responses.
In microglial cells, the cGAS-STING pathway governs innate immune responses to cytosolic nucleic acids, and its hyperactivation contributes to neuroinflammatory pathology. The Sting1 Knockout BV-2 Cell Line enables precise dissection of STING-dependent microglial functions, including activation marker expression, phagocytic clearance, and pro-inflammatory mediator release. This model is particularly valuable for studying conditions driven by aberrant STING activity, such as STING-associated vasculopathy with onset in infancy (SAVI) and neuroinflammatory disorders.
The Sting1 Knockout BV-2 Cell Line supports a wide range of assays, including Western blotting for STING, p-TBK1, and p-IRF3; RT-qPCR for interferon-stimulated genes (Ifnb, Cxcl10, Isg15); ELISA for IFN-?? secretion; and multiplex cytokine profiling. Immunofluorescence can track STING trafficking, and luciferase reporters measure interferon pathway activity. Functional studies such as phagocytosis assays and flow cytometry for microglial activation markers further enable detailed phenotypic characterization. This model is suited for investigations into neuroinflammation, antiviral innate immunity, and cancer immunotherapy. For further inquiries, please contact Ascent Research.