The LRRFIP1 Knockout Raji Polyclonal Cells product provides a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Raji human B lymphoblastoid cell line. Gene disruption of LRRFIP1 is achieved through CRISPR/Cas9-mediated target-gene disruption, yielding a loss-of-function model suitable for investigating LRRFIP1-dependent signaling in a malignant B cell context. This polyclonal format preserves population-level diversity while enabling robust functional studies of the target gene in relevant immune and oncogenic pathways.
The Raji cell line, established from an Epstein-Barr virus (EBV)-positive Burkitt lymphoma patient, is a widely employed B lymphocyte model for lymphomagenesis and viral oncogenesis. These suspension cells maintain EBV in a latent state, resulting in constitutive activation of NF-??B and Wnt cascades, and express surface markers characteristic of mature B cells. Raji cells recapitulate key features of aggressive B cell lymphoma, including rapid proliferation and resistance to apoptosis, making them a rigorous platform for genetic perturbation studies.
LRRFIP1 encodes a multidomain transcriptional repressor and innate immune modulator that competitively binds MyD88 to inhibit TLR-mediated NF-??B signaling. Simultaneously, LRRFIP1 promotes ??-catenin-dependent transcription of IFNB1 and forms complexes with Flightless I (FLII) and Dishevelled (DVL1/2/3) to influence Wnt pathway activity and RAC1-driven cytoskeletal reorganization. Downstream transcriptional targets of LRRFIP1-regulated networks include MYC, CCND1, IL6, and TNF, linking LRRFIP1 function to cell proliferation, inflammation, and structural dynamics in B lymphocytes.
In the Raji B-cell background, LRRFIP1 knockout enables dissection of its role in EBV-driven survival and immune evasion. Abrogation of LRRFIP1 may shift the balance between NF-??B and Wnt/??-catenin signaling outputs, impacting expression of oncogenic drivers such as MYC and cyclin D1. This model is particularly valuable for assessing how LRRFIP1 modulates inflammatory cytokine production and actin cytoskeletal regulation in the context of B cell lymphoma, where dysregulated innate signaling contributes to pathogenesis.
Research applications for this knockout model include functional genomics screening in hematopoietic malignancies, investigation of LRRFIP1??s role in B cell lymphoma proliferation and apoptosis, and validation of LRRFIP1 as a drug target in inflammatory and autoimmune diseases. Typical downstream analyses encompass Western blotting, RT-qPCR, NF-??B dual luciferase reporter assays, TOP/FOP Wnt luciferase reporting, co-immunoprecipitation of LRRFIP1 interactors, flow cytometric profiling of B cell surface markers, and RNA-seq-based transcriptomic profiling. For additional details, please contact Ascent Research.
