The DDB2 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human Raji B-lymphocyte line. These cells harbor a stable disruption of the DDB2 gene introduced by CRISPR/Cas9, resulting in a heterogeneous pool with loss of DDB2 function. The polyclonal format minimizes clonal artifacts, providing a representative model for studying DDB2-dependent mechanisms in a lymphoid background.
Raji cells are an EBV-positive Burkitt’s lymphoma line established from an 11-year-old Nigerian male. As mature B lymphocytes, they are widely used in immunology and cancer research, exhibiting robust proliferation in suspension culture. Their lymphoid origin makes them relevant for examining DNA damage responses and genomic instability in B-cell malignancies.
DDB2 is a key DNA damage recognition factor that specifically binds UV-induced photoproducts. It acts as the substrate receptor for the DDB1?CCUL4A?CRBX1 E3 ubiquitin ligase, which ubiquitinates histones H2A/H3/H4 at damage sites, facilitating chromatin remodeling and recruitment of XPC to initiate global genomic nucleotide excision repair. DDB2 expression is transcriptionally activated by p53, linking DNA repair to tumor suppression. Downstream, it influences p21 and BAX expression, thereby coordinating cell cycle arrest and apoptosis. Interacting partners include PARP1, CBP/p300, and the core NER machinery.
Knockout of DDB2 in Raji cells impairs NER and heightens sensitivity to UV radiation, making this model valuable for dissecting p53-mediated DNA damage responses in B-lymphoma cells. The polyclonal population preserves cellular heterogeneity, enabling robust phenotypic analyses without single-clone bias. This setting is particularly relevant for studying how defective DNA repair contributes to lymphomagenesis and therapy resistance.
Typical applications include UV clonogenic survival assays, ??H2AX immunofluorescence, comet assays, and Western blotting or RT-qPCR for DDB2 and its targets. The cells are suited for xeroderma pigmentosum group E modeling, cancer drug resistance studies, and apoptosis assays (e.g., annexin V). ChIP-qPCR can be used to probe histone modifications at repair foci. For further details, contact Ascent Research.
