The MAPRE1 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population designed for loss-of-function studies of the microtubule plus-end tracking protein EB1. The polyclonal format provides a heterogeneous mixture of Raji B lymphocytes harboring targeted disruptions at the MAPRE1 locus, eliminating the need for clonal isolation. This population model is ideal for bulk assays where average knockout effects are assessed, facilitating rapid functional investigations.
Raji cells are an EBV-positive human Burkitt lymphoma B lymphocyte line derived from an African Burkitt lymphoma patient. These suspension-adapted cells express B-cell markers and carry a c-MYC translocation characteristic of Burkitt lymphoma. They serve as a well-established model for B-cell malignancies, Epstein-Barr virus biology, and lymphomagenesis, offering a robust platform for genetic manipulation and functional readouts of cytoskeletal dynamics in B cells.
MAPRE1 encodes EB1, a core +TIP protein that binds growing microtubule ends and recruits regulatory factors. EB1 is phosphorylated by Aurora kinase A and CDK1, modulating its interactions with scaffolds such as CLIP-170, p150Glued (DCTN1), and APC. Through these complexes, EB1 governs microtubule polymerization, mitotic spindle positioning, and chromosome segregation. It also links microtubules to cortical actin via Rho GTPases and effectors like mDia1, coordinating cell migration and polarity. Additionally, EB1 participates in Wnt signaling through interaction with APC, influencing ??-catenin-dependent transcription.
In Raji B lymphocytes, MAPRE1 knockout permits examination of microtubule-dependent processes central to lymphoma pathophysiology. The EBV-positive background allows researchers to probe EB1’s role in viral episome maintenance and lytic reactivation, which may depend on cytoskeletal reorganization. Disrupted microtubule dynamics can impact proliferation, adhesion, and chemotaxis of malignant B cells, and may alter sensitivity to anti-microtubule agents. This model thus provides a tool to study mitotic vulnerabilities and migration-based dissemination of lymphoma cells.
Applications include live-cell imaging of microtubule growth, mitotic index quantification, transwell migration assays, and co-immunoprecipitation of EB1 interactors. These cells are suited for pharmacologic screens targeting microtubule stabilization or kinase activity, and for elucidating crosstalk between EB1 and Wnt or focal adhesion pathways. For further information, contact Ascent Research.
