The DPYSL5 Knockout Raji Polyclonal Cells constitute a CRISPR/Cas9-mediated loss-of-function model in the Raji B lymphocyte background, engineered to disrupt the DPYSL5 gene, encoding collapsin response mediator protein 5 (CRMP5). This polyclonal knockout cell population provides a genetically heterogeneous pool of edited cells, enabling robust assessment of DPYSL5-dependent phenotypes without isolation of single-cell clones. The product is supplied as a suspension culture of Homo sapiens B cells, ready for functional assays in cytoskeletal biology, signal transduction, and lymphomagenesis research.
The Raji cell line represents an Epstein-Barr virus (EBV)-positive B lymphocyte model derived from a patient with Burkitt’s lymphoma. Widely utilized in immunology and cancer biology, Raji cells display characteristic features of aggressive B-cell malignancies, including rapid proliferation in suspension and competency for cell adhesion, migration, and intracellular signaling studies. Their hematopoietic origin and sustained expression of B-cell markers make them a relevant system for investigating gene functions in lymphomagenesis and immune cell dynamics.
DPYSL5 encodes CRMP5, a cytosolic phosphoprotein that directly interacts with tubulin heterodimers and filamentous actin, thereby regulating microtubule polymerization and actin cytoskeleton remodeling. Its activity is modulated by upstream cues such as Sema3A-mediated activation of the Neuropilin-1/Plexin-A receptor complex, leading to downstream phosphorylation by GSK3?? and Cdk5. Activated CRMP5 orchestrates cytoskeletal rearrangements through Rho GTPases, including RhoA and Rac1, and downstream effectors such as LIMK1 and cofilin, ultimately controlling cell morphology, adhesion, and motility.
In the Raji B-cell context, disruption of DPYSL5 is expected to profoundly alter cytoskeletal architecture, impairing lamellipodia formation, cell migration, and integrin-mediated adhesion. Given the importance of cytoskeletal dynamics in lymphocyte trafficking and B-cell receptor signaling, this knockout model may reveal defects in chemotactic responses and anchorage-independent proliferation. Moreover, because aberrant CRMP5 expression has been associated with lymphoma progression and cancer metastasis, these polyclonal knockout cells serve as a valuable tool for dissecting the cytoskeletal contributions to malignant transformation and immune evasion.
Researchers can employ these cells in a wide range of applications, including transwell migration assays to quantify chemotactic deficits, immunofluorescence analysis of F-actin and tubulin organization, co-immunoprecipitation to map CRMP5 interaction networks with tubulin and actin, and flow cytometry-based proliferation and apoptosis studies using CFSE and Annexin V staining, respectively. The polyclonal nature of the knockout population facilitates functional screening and validation of DPYSL5 as a therapeutic target in B-cell lymphoma. For additional information or custom inquiries, please contact Ascent Research.
