The MAVS Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Raji B lymphocyte line, featuring targeted disruption of the MAVS gene. This loss-of-function model provides a genetically ablated MAVS background for dissecting innate immune signaling without residual MAVS activity.
The Raji host cell line is an Epstein-Barr virus (EBV)-positive Burkitt lymphoma-derived B lymphoblastoid cell line, widely employed for studying B cell receptor signaling, immune responses, and viral interactions. The EBV-positive status makes these cells particularly relevant for investigating viral latency, oncogenesis, and the interplay between herpesvirus infection and host immunity.
MAVS encodes a critical mitochondrial adaptor protein that propagates antiviral signals from cytosolic RNA sensors RIG-I (DDX58) and MDA5 (IFIH1). Upon viral RNA recognition, RIG-I/MDA5 undergo TRIM25-mediated ubiquitination and interact with MAVS on the mitochondrial surface. Activated MAVS forms prion-like aggregates that recruit TRAF3, leading to activation of the kinases TBK1 and IKK??. These kinases phosphorylate transcription factors IRF3 and IRF7, which translocate to the nucleus to drive expression of type I interferons such as IFN-??. Concurrently, MAVS engages TRAF2, TRAF6, and the IKK complex involving NEMO (IKBKG) to activate NF-??B, promoting transcription of pro-inflammatory cytokines including IL-6 and TNF-??. Additional interacting partners such as Tom70 and NLRX1 modulate MAVS function and mitochondrial localization.
In the Raji B lymphocyte context, this MAVS knockout model enables dissection of antiviral innate immunity specific to B cells, which are both responders to and targets of viral infection. EBV-positive lymphoblastoid cells provide a unique backdrop to study how MAVS-dependent signaling influences viral persistence, interferon responses, and potential immune evasion strategies in lymphoma. The polyclonal knockout population preserves genetic heterogeneity, allowing assessment of MAVS contribution across diverse cellular responses without clonal artifacts.
This gene-disrupted cell product supports a broad range of experimental applications, including investigation of RNA virus infection responses (e.g., using vesicular stomatitis virus or Sendai virus), innate immune signaling, and drug screening for antiviral or immunomodulatory compounds. Representative assays compatible with these polyclonal knockout cells include RT-qPCR for interferon and cytokine gene expression, western blot detection of MAVS, phospho-IRF3, and phospho-TBK1, flow cytometry for NF-??B activation, viral replication assays, luciferase reporter assays for IFN-?? or NF-??B activity, immunofluorescence imaging of MAVS aggregation, co-immunoprecipitation for protein interactions, and RNA sequencing to analyze transcriptome changes upon viral stimulation. For further technical details, contact Ascent Research.
