The LY6K Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population derived from the Raji human B lymphocyte line, with targeted disruption of the LY6K gene. This product comprises a heterogeneous pool of cells carrying diverse loss-of-function alterations introduced by non-homologous end joining, enabling studies of gene disruption effects without clonal selection. The polyclonal format reflects the natural variability of CRISPR-Cas9 editing and is suited for bulk analyses of signaling and phenotypic outcomes.
Raji is an Epstein-Barr virus (EBV)-positive Burkitt??s lymphoma B-cell line widely employed in immunology and cancer research. These cells retain key B-lymphocyte characteristics, including surface immunoglobulin expression and antibody production capacity, and serve as an established model for humoral immunity and B-cell malignancies. The line??s well-defined genetic background and responsiveness to extracellular stimuli make it a valuable host for gene knockout studies focused on B-cell receptor signaling and lymphomagenesis.
LY6K encodes a glycosylphosphatidylinositol (GPI)-anchored cell surface protein of the Ly-6/uPAR superfamily, acting as a cancer-testis antigen aberrantly expressed in various carcinomas. It is activated by EGF via EGFR and transcriptionally regulated by Sp1 and demethylating agents. Downstream, LY6K stimulates the PI3K/AKT/mTOR and RAS/RAF/MEK/ERK pathways, resulting in phosphorylation of AKT and ERK1/2, and upregulates Cyclin D1 and MMP-9. The protein interacts with Src family kinases and B-cell receptor complex components within lipid rafts, thereby coupling extracellular cues to proliferation and migration.
In Raji B cells, LY6K is expected to sustain oncogenic signaling through enhanced phospho-AKT and phospho-ERK1/2 levels. Its knockout likely attenuates these pathways, reducing cell proliferation and potentially sensitizing cells to apoptotic stimuli. As a cancer-testis antigen, LY6K loss may also alter tumor immunogenicity by modifying surface molecule interactions or B-cell receptor-associated signaling, providing a model to dissect the interplay between BCR signaling, kinase cascades, and immune evasion in B-cell malignancy.
This polyclonal knockout model is applicable to a variety of experimental assays, including Western blotting and RT-qPCR for expression analysis, flow cytometry for surface LY6K and phospho-protein detection, and functional tests such as MTS proliferation, Transwell migration, and Annexin V apoptosis assays. Transcriptomic profiling by RNA-seq and in vivo xenograft tumor growth studies can further explore global and physiological consequences. These applications support research in cancer biology, B-cell malignancies, immunotherapy target validation, and tumor antigen profiling. For further information, please contact Ascent Research.
