The MYO1B Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population with targeted disruption of the MYO1B gene in Raji B lymphocytes. This loss-of-function model enables study of MYO1B-dependent processes such as actin cytoskeleton dynamics, membrane trafficking, and cell migration. The polyclonal pool reduces clonal artifacts and provides a robust system for functional assays. By eliminating MYO1B expression, researchers can dissect the motor protein’s role in B-cell biology, cancer metastasis, and endocytosis.
The Raji cell line is an EBV-positive Burkitt lymphoma-derived B lymphocyte model that expresses CD19 and CD20 surface markers. Widely used in immunology and cancer research, Raji cells recapitulate features of germinal center B cells and support investigation of B-cell receptor signaling, lymphomagenesis, and therapeutic antibody responses. Their transformed phenotype and constitutive pro-survival signaling make them ideal for studying oncogenic mechanisms in B-cell malignancies and evaluating anti-lymphoma agents.
MYO1B is an unconventional myosin that links actin filaments to cellular membranes, driving endocytosis, migration, and adhesion. It is activated by Rho GTPases including Rac1, Cdc42, and RhoA, and binds phosphoinositides such as PIP2 and calmodulin for membrane targeting. Downstream, MYO1B interacts with actin and endocytic vesicles to generate force for membrane remodeling, functioning within an Arp2/3 complex-associated network that orchestrates dynamic actin reorganization during cell movement and trafficking.
In Raji cells, MYO1B contributes to adhesion, migration, and receptor trafficking, processes central to lymphoma dissemination. Loss of MYO1B in this polyclonal knockout model allows assessment of actin-dependent mechanisms in B-cell spreading, immune synapse formation, and invasive behavior. The model further facilitates investigation of how MYO1B-mediated trafficking modulates surface receptors like CD19 and CD20, which are therapeutic targets, providing insights into cytoskeletal contributions to Burkitt lymphoma malignancy.
These cells enable diverse functional assays, including Transwell migration, adhesion, and transferrin uptake experiments to quantify cell motility and endocytosis. Immunofluorescence staining reveals actin cytoskeletal perturbations, while co-immunoprecipitation validates MYO1B interactions with actin, calmodulin, or PIP2. Western blotting and qRT-PCR confirm knockout efficiency. The knockout model supports high-throughput drug screening for MYO1B pathway inhibitors and investigation of compensatory signaling. For technical details or to request a quote, please contact Ascent Research.
