The FCRLA Knockout Raji Polyclonal Cells are a polyclonal knockout cell population generated from the Raji B lymphocyte line through CRISPR/Cas9-mediated disruption of the FCRLA gene. This loss-of-function model provides a heterogeneous pool of edited cells, enabling robust analysis of FCRLA-dependent processes without the selective bias of clonal expansion.
The parental Raji cell line, derived from a Burkitt lymphoma patient, is EBV-positive and exhibits a type III latency program. As a B lymphoblastoid line, Raji cells express surface IgM and retain the capacity for limited differentiation, making them a widely used system for studying B cell receptor signaling, apoptosis, and lymphomagenesis.
FCRLA encodes an intracellular Fc receptor-like protein that resides predominantly in the endoplasmic reticulum of B cells. It selectively binds IgM heavy and light chains and the ER chaperone BiP/GRP78, forming complexes with GRP94 and ERp57 that regulate immunoglobulin assembly and quality control. FCRLA expression is activated by IL-4 and modulated by B cell receptor stimulation and CD40 signaling. Consequently, FCRLA disruption impairs IgM secretion and alters the expression of plasma cell differentiation markers, linking external activation cues to antibody production.
In the Raji background, FCRLA knockout provides a means to investigate ER-localized immunoglobulin processing in a lymphoma-derived model. The EBV-positive context is particularly relevant for examining how viral latency influences ER stress and immunoglobulin homeostasis. Moreover, the polyclonal nature of the knockout pool allows assessment of population-level heterogeneity, reflecting more physiological variability than monoclonal lines.
Typical research applications include flow cytometry for surface immunoglobulins, western blotting and RT-qPCR for FCRLA and B cell differentiation markers, immunofluorescence, IgM secretion ELISA, and RNA-seq. These approaches support studies of B cell development, antibody production, lymphoma progression, and ER stress pathways. For additional information or technical inquiries, please contact Ascent Research.
