OTUD1 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human Raji B lymphoblast line. This product comprises a heterogeneous pool of cells carrying distinct gene disruptions, generating a loss-of-function model for deubiquitination studies. The polyclonal format supports robust population-level analyses and is well-suited for applications where clonal uniformity is unnecessary, such as pathway screening and drug target validation.
The Raji cell line is a Burkitt lymphoma-derived, EBV-positive human B lymphoblast line widely used in immunology and oncology research. These cells exhibit active NF-??B and interferon signaling and are valued for studying B cell receptor pathways, viral oncogenesis, and apoptosis. Their lymphoblastoid phenotype provides a disease-relevant context for investigating how the deubiquitinase OTUD1 modulates signaling cascades central to B cell survival and transformation.
OTUD1 is a K63-specific deubiquitinase and negative regulator of innate immune signaling. It is activated by TNF-alpha, type I interferons, and viral RNA sensed by RIG-I. OTUD1 cleaves polyubiquitin chains from TRAF3 and TRAF6, attenuating the RIG-I/MAVS/TBK1 axis and TNF-induced NF-??B activation. This reduces IRF3/IRF7 phosphorylation and suppresses expression of interferon-stimulated genes and pro-inflammatory cytokines, thereby dampening inflammation and promoting apoptosis.
In Burkitt lymphoma-derived Raji cells, OTUD1 modulates survival and apoptotic pathways by tempering NF-??B and interferon responses. Knockout of OTUD1 enables dissection of how loss of this deubiquitinase affects TRAF3/6-dependent signaling complexes and alters the balance between proliferation and apoptosis. The EBV-positive Raji background also allows exploration of OTUD1??s role in viral latency and innate antiviral defense, as pattern recognition receptor pathways are often targeted by oncogenic viruses. This polyclonal population captures a range of disruption efficiencies, facilitating studies of graded signaling effects.
Applications include western blotting and phospho-signaling analysis to track pathway activity, NF-??B reporter assays to measure transcriptional output, RT-qPCR for ISG quantification, flow cytometry for apoptosis assessment, co-immunoprecipitation to map interaction networks, and ELISA for cytokine profiling. These assays support research into deubiquitination in B cell lymphoma, inflammation, viral defense, and apoptosis. This knockout model accelerates functional studies and therapeutic target discovery. For further details, contact Ascent Research.
