The CTTNBP2NL Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population designed to disrupt the CTTNBP2NL gene, which encodes a cortactin-binding protein involved in actin cytoskeleton regulation. This gene-edited polyclonal population provides a loss-of-function model in a human B-lymphocyte background, enabling investigation of actin dynamics and signaling pathways in malignant B-cell biology. The polyclonal format preserves cellular heterogeneity while eliminating CTTNBP2NL function across the population, making it suitable for functional genomic studies without single-cell clonal selection.
The host Raji cell line is derived from a Burkitt lymphoma patient and represents an Epstein-Barr virus (EBV)-positive human B lymphocyte model. These suspension-adapted cells robustly express B-cell surface markers including CD19 and CD20, and retain key features of post-germinal center B cells, such as active B-cell receptor (BCR) signaling and antibody production potential. The Raji background is widely used for studying B-cell malignancies, immune synapse formation, and lymphomagenesis due to its transformed phenotype and ease of culture.
CTTNBP2NL functions as a regulator of actin polymerization by binding cortactin and modulating the Arp2/3 complex, a key nucleator of branched actin networks. This protein is activated downstream of BCR signaling and Rho GTPases (Rac1, RhoA, Cdc42) through the PI3K-AKT pathway. It interacts directly with cortactin, F-actin, and the Arp2/3 complex, and has potential associations with SHANK3 and Striatin. By controlling actin branching and polymerization, CTTNBP2NL influences cell migration, adhesion, and membrane protrusion dynamics, processes critical for lymphocyte function.
In Raji B lymphocytes, CTTNBP2NL knockout is expected to compromise actin-dependent events essential for malignant B-cell biology, including BCR clustering, immune synapse assembly, and cell migration. Disruption of cortactin-Arp2/3 regulation may impair cytoskeletal remodeling required for signaling microcluster formation and internalization of the BCR, potentially altering downstream kinase activation and lymphoma cell behavior. This model enables dissection of how cytoskeletal dysregulation contributes to Burkitt lymphoma pathogenesis and metastasis.
Key research applications include functional dissection of BCR-mediated actin remodeling, validation of cortactin?CCTTNBP2NL interaction as a therapeutic target in B-cell malignancies, and screening of cytoskeletal inhibitors. Representative assays supported by this model include Western blotting, RT-qPCR, phalloidin-based F-actin visualization, immunofluorescence for cortactin localization, flow cytometric analysis of BCR clustering, transwell migration assays, cell adhesion assays, phospho-signaling analysis of BCR-proximal kinases, immune synapse reconstitution assays, and BCR internalization assays. For further technical details or to discuss custom applications, please contact Ascent Research.
