The DPYSL2 knockout Raji polyclonal cells are a CRISPR/Cas9-edited polyclonal population derived from Raji B lymphoblasts, carrying disrupted DPYSL2 alleles. This heterogeneous pool preserves genetic diversity, avoiding clonal selection artifacts and providing a robust model for functional assays. The ready-to-use polyclonal knockout cells are supplied from the widely used Raji line, a cornerstone in immunology and oncology research.
Raji cells are a well-characterized human B lymphoblast line originating from a Burkitt lymphoma patient. These EBV-positive cells express B-cell markers (CD19, CD20, MHC II) and grow robustly in suspension, serving as a principal model for B-cell lymphoma biology, EBV-driven oncogenesis, and lymphocyte signaling. Their use in drug screening and cytotoxicity assays highlights their relevance in cancer research.
DPYSL2 encodes CRMP2, a microtubule-associated protein integrating extracellular cues with cytoskeletal reorganization. CRMP2 functions downstream of Sema3A/neuropilin-1/plexin A and is phosphorylated by GSK3??, CDK5, Fyn, and CaMKII. Phosphorylated CRMP2 modulates microtubule dynamics, actin assembly, and endocytosis, controlling migration, axon guidance, and proliferation. CRMP2 directly interacts with tubulin, actin, and kinesin-1, and influences Rho GTPases (RhoA, Rac1, Cdc42) critical for cytoskeletal remodeling.
Disruption of DPYSL2 in Raji B cells is expected to perturb microtubule stability and cell motility, offering a model to study CRMP2 in lymphocyte biology and lymphomagenesis. As CRMP2 is implicated in cancer cell migration and invasion, these knockout cells allow examination of its role in B-cell trafficking, chemotaxis, and lymphoma dissemination. This model also enables exploration of crosstalk between semaphorin signaling and oncogenic PI3K/Akt and GSK3?? pathways.
These DPYSL2 knockout Raji polyclonal cells are suitable for a range of applications, including Western blotting for CRMP2 loss, RT-qPCR, immunofluorescence for microtubule organization, and live-cell imaging of migration. Additionally, they support phospho-signaling arrays, flow cytometry for proliferation and apoptosis, co-immunoprecipitation to map CRMP2 interactomes, and drug sensitivity studies targeting cytoskeletal or kinase pathways. This knockout model serves as a versatile tool for mechanistic studies and preclinical drug target validation in lymphoma and B-cell malignancies. For further information, contact Ascent Research.
