In Stock Cell Lines
Homo sapiens (Human)
Blood (peripheral blood)
Suspension
The MAVS Knockout THP-1 Cell Line is a CRISPR/Cas9-edited human monocytic leukemia cell line featuring targeted disruption of the mitochondrial antiviral signaling adaptor MAVS. Derived from THP-1 cells, this model serves to investigate RIG-I/MDA5-mediated innate antiviral immunity, including pathways involving RIG-I, MAVS, TRAF3, TBK1, IRF3, and NF-??B, and is applicable to research on viral infections, autoimmune disorders, and leukemia. Disruption of MAVS blocks type I interferon and pro-inflammatory cytokine production, enabling dissection of MAVS-dependent signaling. Key applications include viral infection assays, interferon reporter assays, RT-qPCR, ELISA, and drug screening, providing a versatile tool for immunology and oncology research.
LMNB2 Knockout NCI-H1975 Polyclonal Cells
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CEP170 Knockout jurkat Polyclonal Cells
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KLHL7 Knockout HT29 Polyclonal Cells
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P4HA2 Knockout HEK293T Polyclonal Cells
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MET Knockout Raji Polyclonal Cells
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The MAVS Knockout THP-1 Cell Line is a CRISPR/Cas9-edited human monocytic leukemia cell line with targeted disruption of the mitochondrial antiviral signaling protein (MAVS) gene. This knockout model provides a stable loss-of-function system for investigating MAVS-dependent innate antiviral pathways. Derived from the THP-1 cell line, it retains its monocytic characteristics while eliminating MAVS expression, enabling dissection of RIG-I-like receptor (RLR) signaling.
THP-1 is a suspension cell line derived from peripheral blood of a 1-year-old male with acute monocytic leukemia (AML-M5). These cells exhibit monocytic morphology and can be differentiated into macrophage-like cells, serving as a model for monocyte/macrophage biology, immune signaling, and hematological malignancy research. Parental THP-1 cells mount robust RLR-dependent interferon and cytokine responses, providing a relevant context for studying MAVS.
MAVS functions as a mitochondrial adaptor that, upon viral RNA sensing by RIG-I (DDX58) or MDA5 (IFIH1), engages in CARD-CARD interactions with these receptors. This triggers recruitment of TRAF3 and TRAF6, activation of TBK1 and IKK complexes (including NEMO/IKBKG), and subsequent phosphorylation and nuclear translocation of IRF3 and NF-??B. These transcription factors drive expression of type I interferons (IFN??, IFNA), pro-inflammatory cytokines (IL6, TNF), and interferon-stimulated genes (ISG15). MAVS activity is regulated by upstream factors like TRIM25, PACT, and ZAPS, and it interacts with TANK, WDR5, NLRX1, PCBP2, and MFN2. Downstream effectors include IRF3, IRF7, TBK1, IKK??, and ISG15.
In THP-1 cells, MAVS disruption abolishes RIG-I/MDA5-induced antiviral and inflammatory gene expression, making this knockout line critical for dissecting the RLR pathway in a leukemia-relevant context. It enables investigation of cross-talk between antiviral signaling and oncogenic processes, and provides a platform to study viral evasion mechanisms and screen for pathway agonists. By comparing wild-type and knockout responses, researchers can identify MAVS-dependent signaling nodes and explore alternative innate immune pathways.
This cell line is designed for applications in innate immunity, viral pathogenesis, and drug discovery. Standard assays include infection with VSV or SeV, followed by quantification of IFN??, ISG56, and IL6 via RT-qPCR, cytokine measurement by ELISA, or luciferase reporter assays. Western blotting for MAVS and phospho-IRF3 validates knockout and signaling disruption. Additional workflows encompass RNA-seq, flow cytometry for intracellular cytokines, and high-content screening for interferon modulators. It is suitable for studying viral infections (influenza, hepatitis C, SARS-CoV-2), autoimmune diseases (SLE), and leukemia biology. For further technical details or inquiries regarding this MAVS knockout THP-1 cell line, please contact Ascent Research.
