The MAPK6 Knockout Raji Polyclonal Cells represent a genetically engineered cell population generated by CRISPR/Cas9-mediated disruption of the MAPK6 gene in the Raji B lymphocyte cell line (Homo sapiens). This polyclonal knockout model provides a heterogeneous pool of gene-edited cells, each carrying targeted modifications within the MAPK6 locus, enabling the study of loss-of-function effects across a diverse cellular background. The product is supplied as live polyclonal cells, ready for expansion and downstream experimental analysis in advanced biomedical research applications.
The Raji host cell line, originally derived from a patient with Burkitt??s lymphoma, is a well-characterized Epstein-Barr virus (EBV)-positive B lymphocyte model widely used in immunology and oncology research. These cells retain features of mature B cells, including the capacity for robust proliferation and immunoglobulin production, making them a valuable system for investigating B-cell biology, lymphomagenesis, and immune signaling. The EBV-positive status and lymphoma origin provide a unique platform for exploring viral-oncogene interactions and tumor cell signaling pathways.
MAPK6, an atypical mitogen-activated protein kinase, functions in cell cycle progression, differentiation, and cytoskeletal reorganization. It is activated by upstream regulators including PAK1, PAK2, and PAK3, which are effectors of RAC1 and CDC42 in response to growth factors and cellular stress. Activated MAPK6 phosphorylates MAPKAP5, stathmin, and cyclin D1, modulating microtubule dynamics, G1/S transition, and actin remodeling. MAPK6 also interacts with UBE3A, CDC25A, and 14-3-3 proteins, linking it to protein turnover and cell cycle checkpoints.
In Raji B lymphocytes, MAPK6 knockout disrupts signaling networks governing proliferation, survival, and stress responses, offering insights into the role of atypical MAP kinases in B-cell malignancies. Derived from Burkitt??s lymphoma, this cell model is particularly suited for dissecting oncogenic mechanisms such as dysregulated cell cycle control and apoptotic resistance. Additionally, the EBV-positive status permits exploration of crosstalk between viral latency and MAPK6-dependent pathways relevant to lymphoma biology and other cancers.
This polyclonal knockout model supports gene knockout studies, cancer research, B-cell signaling analysis, and drug target validation. Researchers can employ assays like Western blotting, RT-qPCR, co-immunoprecipitation, phospho-signaling analysis, flow cytometry for cell cycle profiling, and migration/invasion assays. RNA-seq enables transcriptomic evaluation of MAPK6 loss. For further details, please contact Ascent Research.
