The LRRFIP2 Knockout Raji Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population designed to disrupt LRRFIP2 gene expression in the Raji B lymphocyte background. This pooled population provides a loss-of-function model for studying LRRFIP2-dependent processes without clonal isolation, enabling efficient protein-level reduction and functional ablation. As a polyclonal preparation, these cells offer reproducible targeting while maintaining population diversity for robust experimental comparisons.
Raji cells, derived from a Burkitt lymphoma, are an established EBV-positive B lymphocyte line extensively used to study B cell biology, including antibody production, antigen presentation, and signal transduction. These cells express characteristic B cell surface markers such as CD19 and CD20 and retain sensitivity to immune stimuli, making them a valuable model for dissecting pathways governing B cell survival, proliferation, and oncogenic transformation.
LRRFIP2 encodes a transcriptional repressor that negatively regulates NF-??B signaling by binding the adaptor protein MYD88, thereby inhibiting TLR-induced activation of IRAK1 and TRAF6 and reducing expression of pro-inflammatory cytokines like IL-6 and TNF. Concurrently, LRRFIP2 interacts with DVL2 to enhance ??-catenin/TCF transcriptional activity, upregulating targets such as MYC and CCND1 and promoting cell proliferation. Upstream activators include TLR agonists (e.g., LPS), Wnt ligands (e.g., Wnt3a), and TNF-??. Through these dual functions, LRRFIP2 critically coordinates innate immune and Wnt/??-catenin pathway outputs.
In Raji cells, LRRFIP2 knockout is predicted to unleash NF-??B-driven pro-inflammatory gene expression while attenuating ??-catenin-dependent proliferative signals, potentially altering cytokine production and cell growth. This dysregulation mirrors pathways implicated in B cell lymphomagenesis and autoimmune conditions such as systemic lupus erythematosus and inflammatory bowel disease, where aberrant NF-??B and Wnt signaling contribute to pathogenesis. Consequently, this model enables investigation of LRRFIP2??s role in malignant B cell transformation and inflammatory responses.
Researchers can employ these cells in luciferase reporter assays for NF-??B and ??-catenin/TCF activity, RT-qPCR for MYC and IL-6, and Western blot to confirm knockout efficiency. Functional studies may include flow cytometry for surface markers CD19 and CD20, apoptosis assessment with Annexin V, cell proliferation assays (MTS), and co-immunoprecipitation of MYD88. Drug screening experiments can evaluate LRRFIP2 pathway-specific sensitivity. For technical enquiries, please contact Ascent Research.
