The MYO1E Knockout Raji Polyclonal Cells product comprises a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Raji B lymphocyte cell line, engineered for loss-of-function studies of the MYO1E gene. This polyclonal pool offers a heterogeneous genetic disruption background, enabling robust functional screening and pathway analysis without clonal bias. The knockout model is produced via CRISPR/Cas9-mediated gene disruption, providing a versatile tool for investigating MYO1E-dependent processes in a human Burkitt lymphoma context.
The Raji cell line is an Epstein-Barr virus (EBV)-positive Burkitt lymphoma B lymphocyte model, widely utilized for studying B cell biology, including antibody production and antigen presentation. Originating from a patient with Burkitt lymphoma, Raji cells retain key features of the adaptive immune response and serve as a system for examining lymphocyte signaling, adhesion, and migration. Their transformed phenotype and EBV-immortalized nature make them a relevant substrate for assessing oncogenic mechanisms and therapeutic interventions.
MYO1E encodes an actin-based motor protein that couples force generation to membrane dynamics, critically regulating clathrin-mediated endocytosis, cell adhesion, and migration. MYO1E localizes to actin-rich structures such as podosomes and invadopodia, where it interacts with binding partners including actin filaments, Tks5, dynamin, synaptojanin, and clathrin to facilitate endocytic vesicle formation and focal adhesion turnover. Upstream, MYO1E is activated by phosphatidylinositol-4,5-bisphosphate (PIP2) and signaling from the Rho GTPases Rac1 and Cdc42, which are triggered by integrin-mediated adhesion. Downstream effectors include reorganization of the actin cytoskeleton and disassembly of focal adhesions, a process mediated in part through FAK and Src kinases. Within the regulatory network, key pathway elements such as integrins, FAK, Src, PIP5K, Rac1, the WAVE complex, Arp2/3, cortactin, and cofilin converge on MYO1E to coordinate cellular motility and adhesive dynamics.
In Raji B lymphocytes, disruption of MYO1E impairs clathrin-mediated endocytosis and focal adhesion turnover, thereby reducing B cell adhesion and transendothelial migration. This phenotype is relevant for lymphoma dissemination studies, as MYO1E-dependent migration and invasion are implicated in cancer metastasis. The model also facilitates investigation of actin-dependent mechanisms linked to focal segmental glomerulosclerosis (FSGS), and the EBV-positive background permits examination of MYO1E’s role in viral latency.
Typical applications include transferrin uptake endocytosis assays, immunofluorescence analysis of F-actin and focal adhesions, and phospho-signaling profiling of FAK/Src by Western blotting. Functional studies employ cell adhesion and Transwell migration assays, while co-immunoprecipitation validates interactions with dynamin, synaptojanin, and clathrin. Flow cytometry monitors surface marker changes. This product also supports cancer cell invasion screening and metastasis inhibitor discovery. For further information or customized services, please contact Ascent Research.
