The CLTA Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population of human Raji B lymphocytes in which the CLTA gene has been disrupted. This loss-of-function model abolishes expression of clathrin light chain A across a heterogeneous cell pool, enabling investigation of clathrin-mediated endocytosis without the constraints of monoclonal selection. The polyclonal format reflects the diversity of editing outcomes while preserving the parental line??s characteristics. It provides a robust platform for studying clathrin-dependent internalization processes in a B-cell context.
The Raji cell line originates from Burkitt??s lymphoma, possessing an EBV-positive background and a c-MYC translocation that drives rapid proliferation. These B lymphocytes retain key immune functions, including antigen presentation and antibody production, making them a relevant model for lymphoma and adaptive immunity research. In this setting, CLTA knockout allows dissection of how clathrin machinery modulates receptor dynamics and signaling in malignant B cells, offering insights into pathways that sustain tumor growth.
CLTA forms heterotrimers with clathrin heavy chain (CLTC) and CLTB, essential for clathrin-mediated endocytosis. It interacts with HIP1, AP-2, epsin, dynamin (DNM1/DNM2), and auxilin to drive vesicle formation. Upstream regulation involves EGFR, transferrin receptor, and AP-2, while downstream cargo includes EGFR, Notch, transferrin receptor, GPCRs, and Toll-like receptors. CLTA knockout disrupts receptor internalization, impairing endosomal trafficking and altering EGFR and Notch signaling pathways, offering a tool to dissect clathrin-dependent trafficking in signal transduction.
In Raji B cells, CLTA knockout impairs antigen internalization and receptor turnover, processes vital for B-cell receptor signaling and immune function. Given that Notch and EGFR signaling intersect with c-MYC-driven proliferation, this model elucidates how endocytic defects may influence lymphoma maintenance. Additionally, clathrin-dependent TLR trafficking impacts innate immune responses in EBV-positive lymphomas. Thus, the knockout cells serve as a valuable tool for exploring the interplay between endocytosis and oncogenic signaling in B-cell malignancies.
These cells are suited for transferrin uptake and EGFR internalization assays, flow cytometric monitoring of surface receptors, and RNA-seq profiling. They enable studies on receptor trafficking, nanoparticle uptake, and drug delivery, alongside functional assays like proliferation and apoptosis measurements. Co-immunoprecipitation and electron microscopy can probe protein interactions. For further information, please contact Ascent Research.
