The DNAJB4 Knockout Raji Polyclonal Cells consist of a Raji B lymphocyte population with CRISPR/Cas9-mediated disruption of the DNAJB4 gene. This polyclonal knockout cell pool, generated without single-cell cloning, retains diverse editing events across the bulk culture, providing a heterogeneous loss-of-function model.
Raji is a human Burkitt??s lymphoma B cell line, EBV-positive, extensively used in immunology and cancer research. These B lymphocytes are characterized by robust immunoglobulin production, antigen presentation, and high proliferative capacity, making them a relevant system for studying lymphomagenesis and B-cell signaling.
DNAJB4 encodes an Hsp40 co-chaperone that activates Hsp70 (HSPA1A) and Hsc70 (HSPA8) ATPase activity, facilitating protein folding, degradation, and ER stress responses. As a p53 target gene, DNAJB4 exerts tumor-suppressive functions by promoting apoptosis via BAX upregulation and cell cycle arrest through p21 induction, while inhibiting EGFR-mediated proliferation and migration. DNAJB4 is transcriptionally regulated by HSF1 under heat shock and participates in the UPR downstream of PERK, IRE1, and ATF6. It also cooperates with STUB1/CHIP to target misfolded substrates for proteasomal clearance, linking chaperone machinery to p53-driven apoptosis and protein quality control.
In the Raji B-cell lymphoma context, DNAJB4 knockout enables dissection of co-chaperone function in malignant B lymphocyte biology, including ER stress adaptation, apoptotic resistance, and EBV-driven proliferation. The polyclonal knockout population recovers a range of editing events, mirroring intratumoral heterogeneity and allowing genotype?Cphenotype correlation without clonal bias. Additionally, Raji cells?? active antibody secretion and antigen presentation facilitate studies on the role of chaperones in immunoglobulin biosynthesis and immune recognition.
Research applications include Western blotting and RT-qPCR to confirm DNAJB4 loss and evaluate downstream targets (p21, BAX), co-immunoprecipitation to probe Hsp70?Cclient interactions, and flow cytometric Annexin V assays for apoptosis quantification. Tunicamycin-induced ER stress assays reveal DNAJB4??s role in UPR regulation, while migration and proliferation assays measure its impact on tumor cell behavior. The model also supports small-molecule screening for agents targeting proteotoxic stress or p53 reactivation in B-cell malignancies. For technical inquiries, please contact Ascent Research.
