The LRRC8E Knockout Raji Polyclonal Cells comprise a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human Raji B lymphocyte cell line. This population carries targeted disruption of the LRRC8E gene, which encodes a subunit of the volume-regulated anion channel (VRAC). The polyclonal format provides a genetically diverse loss-of-function model arising from CRISPR-mediated gene disruption, avoiding clonal selection bias. This product is optimized for functional investigations of LRRC8E in B cell volume regulation and associated signaling networks.
Raji cells are an established B lymphocyte model originating from Burkitt lymphoma, retaining mature B cell characteristics including surface immunoglobulin expression and robust proliferative capacity. They are extensively utilized in immunology and oncology for studies on B cell activation, antigen presentation, apoptosis, and malignant transformation. The lymphoblastoid nature of Raji cells offers a reproducible and scalable platform for gene knockout experiments aiming to elucidate immune cell signaling and cancer biology.
LRRC8E is an essential subunit of the heteromeric VRAC complex, which also includes LRRC8A, LRRC8B, LRRC8C, and LRRC8D. This complex functions as an osmosensor, opening under hyposmotic stress to mediate chloride and organic osmolyte efflux, driving regulatory volume decrease (RVD). Activation is regulated by hyposmotic conditions, reactive oxygen species, and Src family kinases. Downstream, VRAC controls chloride conductance and osmolyte transport, influencing apoptosis and proliferation. LRRC8E thus links osmotic cues to intracellular signaling for lymphocyte volume homeostasis.
Knockout of LRRC8E in Raji B cells is predicted to abolish VRAC-mediated RVD, sensitizing cells to osmotic stress and potentially perturbing B cell receptor signaling and apoptotic pathways. As VRAC is implicated in immune cell function, LRRC8E disruption may impair normal B lymphocyte physiology and contribute to phenotypes relevant to B cell malignancies and immunodeficiency. This model enables dissection of how volume-sensitive anion currents intersect with B cell signal transduction, offering insights into lymphoma pathogenesis and immune dysregulation.
This knockout population supports patch clamp electrophysiology for VRAC current measurement, fluorescence-based anion flux assays, cell volume analysis, flow cytometry for apoptosis, and Western blotting and proliferation assays. These techniques facilitate investigations into ion channel function, osmotic stress responses, and B cell pathophysiology, with direct relevance to immunology and cancer research. For further information, please contact Ascent Research.
