In Stock Cell Lines
The MAVS Knockout MDBK Cell Line is a CRISPR/Cas9-edited knockout cell line derived from Madin-Darby bovine kidney (MDBK) cells. It features targeted disruption of the MAVS gene, which encodes a critical mitochondrial adaptor protein that activates IRF3 and NF-??B downstream of the RNA sensors RIG-I and MDA5. This model abolishes MAVS-dependent type I interferon induction, enabling dissection of innate antiviral signaling pathways in a bovine epithelial background. It supports viral replication studies, host-pathogen analyses, and antiviral screening. It is particularly suited for investigating bovine viral infections and evaluating MAVS role in interferon responses using Western blotting, RT-qPCR, and viral replication assays.
NPTX2 Knockout Hela Polyclonal Cells
Cat. No. ARG9048
KDM5A Knockout K562 Polyclonal Cells
Cat. No. ARG20757
ACBD6 Knockout SK-HEP-1 Polyclonal Cells
Cat. No. ARG32070
DIXDC1 Knockout HAP1 Polyclonal Cells
Cat. No. ARG38815
ABCD4 Knockout huh-7 Polyclonal Cells
Cat. No. ARG27741
OACP4 C
Cat. No. ARC0679
The MAVS Knockout MDBK Cell Line is a CRISPR/Cas9-edited knockout cell line in which the gene encoding mitochondrial antiviral-signaling protein (MAVS) has been disrupted. This model provides a powerful tool for dissecting innate immune signaling pathways dependent on MAVS, particularly the RIG-I-like receptor (RLR) pathway. By eliminating functional MAVS expression, the cell line enables researchers to examine MAVS-dependent antiviral responses, viral replication dynamics, and the role of mitochondrial adaptors in host defense.
The parental MDBK cell line is an immortalized bovine kidney epithelial cell line derived from adult Bos taurus kidney. MDBK cells are widely utilized in virology research, especially for propagation and study of viruses that infect cattle, including bovine viral diarrhea virus, bovine herpesvirus, and influenza viruses. Their robust growth characteristics and permissiveness to various viral pathogens make them an ideal host for investigating host-pathogen interactions in a relevant livestock species.
MAVS is an essential adaptor protein resident on the mitochondrial outer membrane that acts downstream of cytosolic RNA sensors RIG-I (DDX58) and MDA5 (IFIH1). Upon viral RNA recognition, MAVS aggregates and recruits TRAF3, TRAF6, and the kinases TBK1 and IKK??, leading to phosphorylation and nuclear translocation of IRF3 and IRF7 transcription factors. These events drive the expression of type I interferons (IFN-?? and IFN-??) and interferon-stimulated genes (ISGs), establishing an antiviral state. MAVS also interfaces with NF-??B signaling, further amplifying the immune response. Negative regulators, such as NLRX1, modulate MAVS activity to prevent excessive inflammation.
In the context of bovine kidney epithelium, MAVS plays a critical role in mediating innate immune responses against RNA viruses that target renal and other tissues. This knockout model enables the study of bovine-specific immune signaling, which can differ from human or murine systems. It serves as a valuable tool for understanding how viral pathogens evade host immunity in cattle, assessing the contribution of MAVS to interferon production and cell-autonomous defense, and evaluating the impact of MAVS loss on viral replication and pathogenesis.
Typical research applications include evaluating IRF3 phosphorylation by Western blotting, quantifying IFN-?? and ISG induction via RT-qPCR, and measuring viral replication kinetics in the absence of MAVS. Luciferase reporter assays using the IFN-?? promoter can assess signaling defects, while co-immunoprecipitation and immunofluorescence microscopy allow examination of MAVS interactors and mitochondrial localization. The line is also suitable for antiviral drug screening and vaccine development studies targeting RLR-dependent pathways. For further details, please contact Ascent Research.
