The MAP2K6 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population of Raji B lymphocytes with targeted disruption of the MAP2K6 gene. This heterogeneous pool allows study of MAP2K6 loss-of-function without clonal artifacts, providing a broad model for acute signaling and phenotypic analyses in a suspension B cell system.
The Raji cell line is an EBV-positive human Burkitt lymphoma B cell line that grows in suspension. It serves as a well-established model for B cell malignancies, EBV latency, and immune cell interactions. Raji cells express key B cell markers and are suitable for genetic manipulation, making them a relevant host for investigating B cell receptor signaling and oncogenic pathways.
MAP2K6 is a dual specificity kinase that activates the p38 MAPK subfamily by phosphorylating MAPK14 (p38alpha) and MAPK11 (p38beta) in response to inflammatory stimuli. Upstream activators include MAP3K5 (ASK1) and MAP3K7 (TAK1), triggered by TNF-alpha, IL-1beta, and Toll-like receptor ligands. Downstream, p38 phosphorylates transcription factors ATF2, MEF2C, and ELK1, driving expression of pro-inflammatory cytokines. MAP2K6 also interacts with TAB1 and forms complexes with MAP3K5, MAP3K7, and MAPK14, integrating signals from TNF, IL-17, and NOD-like receptor pathways.
In Raji B cells, MAP2K6-mediated p38 activation regulates inflammatory gene expression, apoptosis, and differentiation. Dysregulated p38 signaling is associated with Burkitt lymphoma and inflammatory diseases like rheumatoid arthritis and inflammatory bowel disease. Knockout of MAP2K6 in this context enables dissection of its specific role in B cell stress responses and EBV-driven transformation, offering a platform to examine kinase dependency in lymphoid malignancies.
Applications include quantification of p38 phosphorylation by Western blotting and phospho-antibody arrays, measurement of cytokine transcription via RT-qPCR, and flow cytometry for B cell activation markers. Proliferation and apoptosis assays permit functional phenotyping, while inhibitor studies can probe compensatory signaling. This polyclonal knockout population is ideal for initial target validation in inflammatory disease and cancer drug discovery. For further information, contact Ascent Research.
