The LCP1 Knockout Raji Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal knockout cell population generated from the human Raji B lymphocyte line. Through CRISPR/Cas9-mediated disruption of the LCP1 gene, these cells lack functional L-plastin, providing a versatile loss-of-function model. The polyclonal format preserves genetic heterogeneity, making it suitable for experiments where bulk assessment of L-plastin-dependent processes is prioritized over clonal uniformity.
The Raji cell line is an Epstein-Barr virus (EBV)-positive B lymphoblastoid line derived from a patient with Burkitt lymphoma. It retains key B-cell attributes including surface immunoglobulin expression and robust responsiveness to B cell receptor (BCR) and chemokine cues. As a well-established model for B-cell signaling, immune synapse formation, and lymphomagenesis, Raji cells offer a reproducible platform for studying L-plastin function in a malignant B-cell context.
L-plastin, encoded by LCP1, is an actin-bundling protein that organizes F-actin into parallel bundles, thereby regulating cytoskeletal dynamics in lymphocytes. Following BCR engagement or chemokine receptor activation, signaling through Syk, PKC, and Rho GTPases Rac1 and Cdc42 drives L-plastin phosphorylation and its recruitment to the immunological synapse and cell leading edge. L-plastin interacts with F-actin and adhesion components such as integrin LFA-1, vinculin, and talin, working alongside Vav1 to reinforce cell adhesion and promote lamellipodia formation. Consequently, L-plastin is essential for immune synapse stabilization, antigen internalization, and directed cell migration in response to chemotactic gradients.
Loss of LCP1 in Raji cells disrupts the actin-bundling activity required for immune synapse assembly, antigen uptake, and integrin-mediated adhesion. This knockout model recapitulates cytoskeletal defects linked to immunodeficiencies and reveals vulnerabilities in B-cell malignancies where L-plastin is frequently overexpressed. Given the Raji cell’s Burkitt lymphoma origin, LCP1 disruption provides a tractable system to dissect how actin remodeling contributes to lymphomagenesis, tumor cell dissemination, and therapeutic resistance.
This polyclonal knockout cell product is compatible with a range of assays, including Western blotting, immunofluorescence, and flow cytometry for protein-level analysis, as well as Transwell migration, calcium flux, and co-immunoprecipitation to probe functional and protein-interaction networks. RNA-seq can further elucidate transcriptomic changes resulting from L-plastin ablation. Researchers exploring BCR signaling, chemokine-mediated migration, immune synapse architecture, or targeting of L-plastin in B-cell lymphomas and autoimmune diseases will find these cells highly relevant. For additional information, please contact Ascent Research.
