MYH14 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population lacking functional MYH14. This product provides a heterogeneous pool of Raji B lymphocytes with targeted disruption of the gene encoding non-muscle myosin heavy chain II-C, enabling loss-of-function studies in a suspension-adapted human Burkitt’s lymphoma background.
Raji cells are immortalized human B lymphocytes originating from Burkitt’s lymphoma, characterized by Epstein-Barr virus (EBV) positivity and suspension growth. As professional antigen-presenting cells, they participate in antibody production and immune surveillance, making them an ideal model for studying B cell biology, lymphomagenesis, and immune synapse dynamics.
MYH14 encodes the heavy chain of non-muscle myosin II-C, an actin-based motor protein that cross-links filamentous actin (F-actin) and generates contractile forces essential for cell migration, adhesion, and cytokinesis. The activity of myosin II-C is regulated by upstream Rho GTPase signaling, with activation promoted by RhoA and its effector ROCK1, as well as by Ca2+/calmodulin and Rac1. This motor protein interacts with actin filaments and regulatory light chains such as MYL9 and MYL12B, and its function couples to focal adhesion components including vinculin and paxillin. MYH14-mediated actomyosin contraction is integrated within the actin cytoskeleton regulation and focal adhesion pathways, transmitting mechanical signals that govern cellular morphology and motility.
In B lymphocytes, MYH14-dependent actomyosin dynamics are critical for cell polarization, directed migration, and formation of the immune synapse. Disruption of MYH14 in the Raji polyclonal knockout population impairs these processes, providing a model to investigate the cytoskeletal basis of B cell immune responses. This has direct relevance to autosomal dominant deafness DFNA4, where MYH14 mutations cause hearing loss, as well as to peripheral neuropathy and breast cancer metastasis, conditions associated with aberrant cell motility and adhesion.
The MYH14 Knockout Raji Polyclonal Cells support diverse experimental approaches, including Western blotting and immunofluorescence microscopy to verify MYH14 loss and assess compensatory myosin isoforms. Functional studies can employ migration and invasion assays (e.g., Transwell), wound healing assays, and flow cytometry to quantify changes in surface adhesion molecules. Co-immunoprecipitation experiments enable dissection of MYH14 interactomes involving actin, calmodulin, and regulatory light chains. Together, these assays facilitate investigations into hearing loss mechanisms, cancer cell motility, cytoskeletal architecture, and immune synapse formation in B lymphocytes. For inquiries regarding this product, please contact Ascent Research.
