The PDLIM2 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Raji B-lymphocyte line, providing a loss-of-function model for PDLIM2. This heterogeneous pool of cells harbors targeted gene disruptions, enabling bulk functional studies without single-cell cloning, and is ideal for analyzing PDLIM2-dependent processes in a relevant lymphoid context.
The Raji host cell line is a human B-lymphoblastoid line established from a Nigerian patient with Burkitt lymphoma. These EBV-positive cells feature constitutive NF-??B activity and are widely used in immunology and cancer research to investigate B-cell malignancies, viral oncogenesis, and signal transduction pathways. Their lymphoblastoid nature makes them a pertinent model for studying tumor suppressor mechanisms in lymphoma.
PDLIM2, an E3 ubiquitin ligase, targets NF-??B p65 (RELA) for polyubiquitination and proteasomal degradation, thereby attenuating NF-??B signaling. It is induced by TNF-?? and LPS via NF-??B feedback, and its loss leads to accumulation of p65 and enhanced expression of targets like IL6, IL8, and BCL2. PDLIM2 interacts with RELA, actin, and proteasomes, and operates within a network including NFKB1, IKBKB, and IKBKG, suppressing B-cell proliferation and survival as a tumor suppressor.
In Raji lymphoma cells, PDLIM2 knockout amplifies NF-??B activity, driving increased survival and proliferation, thus modeling key aspects of lymphomagenesis. This system is valuable for dissecting negative feedback that limits NF-??B in B cells and for studying how EBV hijacks host pathways. It provides a platform to elucidate tumor-suppressive functions and oncogenic signaling in a disease-relevant background.
Applications include Western blotting for p65 levels, NF-??B reporter assays, ubiquitination assays, and co-immunoprecipitation to assess protein interactions. Functional outcomes such as proliferation and apoptosis can be measured, and RNA-seq can profile NF-??B target gene expression. This model supports research into lymphoma, inflammatory signaling, negative feedback mechanisms, and B-cell biology. For further inquiries, please contact Ascent Research.
