The MYH10 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-mediated gene-disrupted polyclonal population derived from the human Raji B lymphocyte line, targeting the MYH10 locus encoding non-muscle myosin heavy chain IIB (NMHC IIB). This product provides a heterogeneous pool of knockout cells, enabling robust loss-of-function analysis of NMHC IIB in a lymphoid background without clonal selection. The polyclonal format preserves diverse genetic modifications across the cell population, facilitating studies that require physiological variability while avoiding artifacts from single-cell clone expansion.
The Raji cell line, originally established from a Burkitt lymphoma patient, is an Epstein-Barr virus (EBV)-positive suspension lymphoblastoid model widely used in B lymphocyte biology research. Raji cells retain key features of B-cell signaling, antigen presentation, and transformed growth, making them an ideal platform for investigating oncogenic mechanisms, immune cell dynamics, and cytoskeletal regulation. Their lymphoblastoid nature supports high-throughput screening and detailed cell-based assays in suspension, offering a clinically relevant context for MYH10 functional analysis in B-cell malignancies.
MYH10 encodes NMHC IIB, a motor protein that assembles with myosin light chains (MLC) to form myosin II hexamers, which bind and contract actin filaments. This contractile activity is central to cytokinesis, cell migration, adhesion, and maintenance of cellular architecture. NMHC IIB functions downstream of RhoA GTPase and its effector ROCK kinase, which phosphorylate MLC and MYL9, promoting actomyosin assembly; additionally, MLCK and TGF-??/SRF signaling transcriptionally regulate MYH10 expression. NMHC IIB interacts directly with actin, tropomyosin, calmodulin, and focal adhesion components including talin, vinculin, FAK, and paxillin, thereby linking contractility to focal adhesion turnover and integrin-mediated adhesion.
In Raji B lymphocytes, MYH10-driven actomyosin forces are critical for functional behaviors such as cell migration and cytokinesis, processes often dysregulated in lymphoma progression and metastasis. Disruption of MYH10 in this model provides a powerful tool to dissect how non-muscle myosin IIB contributes to B-cell tumor cell invasion, adhesion dynamics, and division. The polyclonal knockout population enables researchers to study the collective impact of MYH10 loss on RhoA/ROCK-dependent pathways within a heterogeneous cancer cell population, reflecting the complexity of in vivo tumor biology.
This MYH10 Knockout Raji product supports diverse investigative applications, including assessment of cell migration via transwell assays, cytokinesis analysis by time-lapse microscopy, and evaluation of focal adhesion architecture through immunofluorescence for actin and vinculin. Researchers can validate target disruption via western blotting and examine downstream signaling by phospho-MLC staining or RhoA activation assays. Flow cytometric cell cycle profiling and adhesion assays further enable comprehensive functional genomics studies of actomyosin contractility in B-cell models, contributing to drug discovery efforts in oncology and neurodevelopmental disorders. For further information, contact Ascent Research.
