The MYO1F Knockout Raji Polyclonal Cells product comprises a CRISPR/Cas9-edited polyclonal knockout population with targeted disruption of the MYO1F gene in the Raji B lymphocyte line. This polyclonal format provides a genetically diverse loss-of-function model, free from single-clone artifacts, enabling robust investigation of MYO1F in B cell biology. The CRISPR-mediated gene disruption technique ensures efficient knockout across the population, making it suitable for assays requiring bulk cellular responses.
Raji cells are an Epstein-Barr virus (EBV)-positive mature B lymphocyte line originating from Burkitt??s lymphoma, characterized by the t(8;14) translocation that leads to c-MYC overexpression. These cells serve as a paradigm for studying B cell receptor (BCR) signaling, mechanisms of lymphomagenesis, and EBV-associated B cell transformation. Their mature B cell phenotype supports the study of immune synapse formation, adhesion dynamics, and migratory behavior, all critical for understanding B cell activation and malignancy.
MYO1F encodes an unconventional myosin that serves as a key link between BCR activation and actin cytoskeleton remodeling. It is activated by the small GTPases RAC1, CDC42, and RHOA, as well as by calcium and calmodulin. Upon BCR engagement, SYK- and BTK-dependent signaling triggers PLC??2 and the VAV guanine nucleotide exchange factor, leading to RAC1 activation. Active RAC1 recruits MYO1F to the cortical actin network, where it interacts with actin filaments, calmodulin, and the ARP2/3 complex to promote F-actin polymerization and integrin-mediated adhesion. This process drives B cell spreading, immune synapse maturation, and antigen internalization, positioning MYO1F as a critical mediator of immune cell adhesion and migration.
In the Raji context, MYO1F disruption enables the dissection of its contributions to adhesion, migration, and synaptic architecture, processes that are implicated in Burkitt??s lymphoma aggressiveness, autoimmunity, and immunodeficiency disorders. This knockout model helps elucidate how BCR-driven cytoskeletal dynamics influence tumor cell dissemination, immune synapse stability, and interactions with the microenvironment, providing a platform for exploring the molecular basis of B cell malignancies and related diseases.
Research applications encompass phospho-signaling analysis and Western blotting to map BCR pathway activation, immunofluorescence for visualizing synaptic actin and adhesion complexes, and quantitative cell adhesion and migration assays. The polyclonal knockout pool is also well-suited for transcriptomic profiling by RNA-seq, enabling genome-wide insights into MYO1F-dependent gene regulation. Additional uses include drug screening to identify modulators of cytoskeletal pathways in B cell diseases and evaluation of therapeutic targets. For further information or to discuss custom requests, please contact Ascent Research.
