In Stock Cell Lines
Mus musculus (Mouse)
Ascites
Adherent
The Mavs Knockout RAW 264.7 Cell Line is a CRISPR/Cas9-edited macrophage cell line lacking expression of MAVS, the central mitochondrial adaptor for innate antiviral immunity. Disruption of Mavs abolishes signaling downstream of RIG-I and MDA5, preventing activation of IRF3 and NF-??B, and thereby blocking production of type I interferons and proinflammatory cytokines. This knockout model is ideal for studying RLR-mediated antiviral responses, viral infection mechanisms, and MAVS-dependent signaling networks. Applications include viral assays, cytokine profiling, and drug screening in a macrophage background. For details, contact Ascent Research.
MR1 Knockout Hela Polyclonal Cells
Cat. No. ARG8256
C5orf24 Knockout jurkat Polyclonal Cells
Cat. No. ARG41516
EHMT2 Knockout HAP1 Polyclonal Cells
Cat. No. ARG40872
DYNLT3 Knockout HEK293T Polyclonal Cells
Cat. No. ARG40188
COL5A1 Knockout HEK293T Polyclonal Cells
Cat. No. ARG4218
MSTO-211H
Cat. No. ARC0545
The Mavs Knockout RAW 264.7 Cell Line is a CRISPR/Cas9-edited knockout cell line in which the Mavs gene has been disrupted, providing a loss-of-function model to dissect MAVS-dependent innate antiviral signaling. Derived from the RAW 264.7 murine macrophage line, this product enables researchers to investigate mitochondrial antiviral-signaling protein (MAVS) function in a homogeneous, genetically defined background without endogenous gene expression interference.
RAW 264.7 cells are a BALB/c mouse-derived macrophage cell line transformed with Abelson leukemia virus. As professional phagocytes, they exhibit robust phagocytic activity and secrete a wide array of cytokines upon activation, making them a widely used model for studying macrophage biology, innate immunity, and host-pathogen interactions. Their rapid growth and ease of transfection further facilitate high-throughput genetic and pharmacological studies.
MAVS is an essential adaptor protein localized to the mitochondrial outer membrane. Upon cytosolic detection of viral RNA by RIG-I-like receptors (RLRs) such as RIG-I (DDX58) and MDA5 (IFIH1), MAVS undergoes oligomerization and recruits signaling complexes involving TRAF3, TRAF6, TBK1, and IKK??. This leads to phosphorylation and nuclear translocation of transcription factors IRF3 and IRF7, which drive type I interferon (IFN-??/??) production, while TRAF6 and the IKK complex activate NF-??B, inducing proinflammatory cytokines including IL-6 and TNF-??. MAVS also interacts with regulatory proteins such as NLRX1, MFN1, MFN2, TRADD, FADD, RIP1, and NEMO, integrating signals to tailor antiviral and inflammatory responses.
In RAW 264.7 macrophages, MAVS is critical for mounting effective innate immune responses against RNA viruses detected by the RIG-I/MDA5 pathway. Disruption of Mavs in this cell line ablates downstream IRF3/NF-??B activation, severely impairing IFN-?? induction and cytokine secretion, and rendering the cells permissive to viral replication. This knockout model thus provides a powerful tool to examine MAVS-dependent host defense mechanisms, viral evasion strategies, and the crosstalk between antiviral and inflammatory pathways in a physiologically relevant macrophage context.
This cell line supports a broad range of applications, including viral infection assays with Sendai virus, influenza, and VSV; RT-qPCR analysis of IFN-??, ISG56, and cytokine transcripts; Western blotting for phosphorylated IRF3 and TBK1; luciferase reporter assays for the IFN-?? promoter; immunofluorescence imaging of MAVS aggregation; flow cytometry for intracellular cytokines; ELISA for secreted IFN-?? and IL-6; and RNA-seq transcriptomic profiling. It is also suitable for antiviral drug screening and identifying MAVS interactors. For further information, contact Ascent Research.
