The MAP3K7 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population designed to disrupt MAP3K7 expression in the human Raji B lymphoblastoid cell line. This loss-of-function model enables study of TAK1 ablation in a lymphoid background. The polyclonal format provides a heterogeneous pool of edited cells, suitable for population-level assays and functional screens.
The Raji cell line is a Burkitt lymphoma-derived B lymphoblastoid line established from a pediatric patient. These cells maintain key characteristics of B lymphocytes, including the capacity for antibody production and antigen presentation, making them a widely used model for B cell biology, immunology, and hematopoietic malignancies. Their rapid proliferation and well-characterized signaling networks facilitate reproducible studies of kinase cascades and transcriptional regulation in a lymphocytic context.
MAP3K7 encodes TAK1 (transforming growth factor-beta-activated kinase 1), a serine/threonine kinase that functions as a central node in multiple signal transduction pathways. TAK1 is activated by upstream receptors and adaptor proteins, including IL-1 receptor, TNF receptor, Toll-like receptors, TGF-??, and Wnt ligands, through complex formation with TAB1, TAB2, TAB3, and TRAF6. Activated TAK1 phosphorylates and activates the IKK complex??leading to NF-??B nuclear translocation??and simultaneously triggers MAP kinase cascades, resulting in JNK and p38 phosphorylation and subsequent AP-1 transcription factor activation. This coordinated signaling regulates the expression of pro-inflammatory cytokines, anti-apoptotic factors, and genes involved in cell survival and immune responses.
In Raji cells, TAK1 signaling intersects with B cell receptor pathways and lymphoma networks, influencing NF-??B and MAPK activity often dysregulated in lymphomagenesis. MAP3K7 disruption allows dissection of TAK1-dependent versus -independent signaling, particularly pro-survival and inflammatory gene programs. Since TAK1 mediates responses to IL-1 and TNF-??, these knockout cells clarify how B lymphoblastoid cells modify apoptotic thresholds, proliferation, and immune functions without functional TAK1.
Applications include mechanistic studies of NF-??B and MAP kinase pathways, cancer research on Burkitt lymphoma and B cell malignancies, and inflammatory disease modeling. Compatible assays include western blotting for phospho-TAK1, NF-??B luciferase reporter analysis, phospho-p38/JNK ELISA, RT-qPCR for target genes, apoptosis flow cytometry, co-immunoprecipitation of TAB1-TAK1 complexes, and cytokine release assays. This polyclonal model supports high-throughput TAK1 inhibitor screening and comparative omics. For additional information, contact Ascent Research.
