The CREB3L4 Knockout Raji Polyclonal Cells represent a CRISPR/Cas9-mediated polyclonal knockout cell population derived from the Raji B lymphocyte line, designed for functional studies of the ER stress sensor transcription factor CREB3L4. This polyclonal product provides a heterogeneous gene-disrupted pool in which CREB3L4 expression is ablated across the population, enabling robust loss-of-function experiments without the clonal selection biases inherent to single-cell-derived lines. Researchers can use these cells to interrogate CREB3L4-dependent signaling events in B-cell contexts.
Raji cells are an Epstein-Barr virus (EBV)-positive Burkitt lymphoma-derived B lymphoblastoid line extensively used in immunology and cancer research. Originating from a patient with Burkitt lymphoma, these cells maintain many features of germinal center B cells and serve as a workhorse model for studying B-cell malignancies, antigen presentation, and apoptotic pathways. Their robust growth in suspension and well-characterized signaling networks make Raji cells particularly suitable for CRISPR-based functional genomic screens and detailed biochemical analyses.
The CREB3L4 gene encodes an endoplasmic reticulum (ER)-resident transcription factor that functions as a key sensor of proteotoxic stress. Under basal conditions, CREB3L4 is retained in the ER membrane through interaction with the chaperone GRP78/BiP. Upon accumulation of misfolded proteins, CREB3L4 dissociates from BiP, traffics to the Golgi apparatus, and undergoes sequential cleavage by Site-1 protease (S1P) and Site-2 protease (S2P). This regulated intramembrane proteolysis releases the N-terminal cytoplasmic domain, which translocates to the nucleus and transcriptionally activates unfolded protein response (UPR) target genes, including HSPA5 (BiP), HERPUD1, XBP1, and CHOP/DDIT3. CREB3L4 thus operates within the ATF6 branch of the UPR, integrating ER stress signals with transcriptional outputs alongside IRE1 and PERK sensors.
In the Raji B-cell lymphoma context, CREB3L4??s role in ER stress adaptation is particularly relevant given the high secretory demands of B lymphocytes and the oncogenic stress inherent in Burkitt lymphoma. EBV-driven proliferation and sustained immunoglobulin expression impose chronic ER stress, likely engaging UPR pathways for survival. Ablating CREB3L4 in this polyclonal knockout population permits dissection of its specific contribution to UPR-mediated cytoprotection, apoptosis regulation, or drug sensitivity. This model can reveal whether CREB3L4 acts as a pro-survival factor in lymphoma cells and may identify vulnerabilities exploitable by ER stress-modulating agents.
These CREB3L4 knockout Raji polyclonal cells support various functional assays. ER stress inducers such as tunicamycin or thapsigargin can be applied, with downstream analysis by Western blotting, RT-qPCR, or immunofluorescence to assess UPR activation. Flow cytometry enables quantification of apoptosis and proliferation, while RNA-seq can define the CREB3L4-dependent transcriptome. This model is valuable for functional genomics, drug screening, and mechanistic studies in B-cell lymphoma. For further information, please contact Ascent Research.
