The DPP8 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population derived from Raji B lymphocytes, with disruption of the DPP8 gene to create a loss-of-function model for functional studies. This polyclonal format provides a heterogeneous knockout pool, avoiding clonal bias and enabling robust pathway analysis.
Raji is a suspension EBV-positive Burkitt lymphoma cell line expressing surface IgM and B-cell markers, widely used to study B-cell biology, lymphomagenesis, and immune signaling. Its malignant B-cell phenotype and well-characterized signaling pathways make it an ideal host for investigating oncogenic mechanisms and therapeutic interventions.
DPP8 is a dipeptidyl peptidase that processes N-terminal dipeptides from substrates involved in immune activation, apoptosis, adhesion, and inflammation. In Raji cells, DPP8 is regulated by NF-??B, Wnt/??-catenin, and B-cell receptor signals, and modulates downstream targets such as chemokines CXCL10, CCL2, CXCL12, caspase-9, and PARP1. DPP8 interacts with CARD8, NLRP1, and DPP9, and its disruption may relieve CARD8-mediated inhibition of the NLRP1 inflammasome, promoting caspase-1 activation and pyroptosis. Additionally, DPP8 influences ??-catenin stability and TCF/LEF-mediated transcription.
In Raji lymphoma cells, DPP8 knockout enhances apoptosis via increased caspase-3 and PARP1 cleavage, and potentially engages inflammasome-dependent cell death through CARD8/NLRP1. Dysregulated chemokine processing alters migratory behavior and immune interactions, while Wnt pathway changes affect proliferation. These phenotypes underscore the model??s utility for studying B-cell lymphoma survival, inflammasome biology, and crosstalk between cell death and oncogenic signaling.
This polyclonal knockout model supports diverse experimental applications including Western blotting, flow cytometry, RT-qPCR, ELISA, chemotaxis, co-immunoprecipitation, and RNA-seq. It enables investigation of DPP8 roles in B-cell lymphoma, immune cell activation, apoptosis, and inflammasome regulation, and serves as a platform for validating DPP8-targeted inhibitors. For additional information, please contact Ascent Research.
