MAP2K4 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Raji B lymphocyte cell line. This product features targeted disruption of the MAP2K4 gene, resulting in a loss-of-function model for studying the dual-specificity MAP kinase kinase in B-cell contexts. The polyclonal nature provides a heterogeneous pool of knockout cells, enabling robust population-level analyses without clonal bias. These cells serve as a versatile tool for investigating stress-activated kinase signaling and cytokine responses.
The parental Raji cell line is an EBV-transformed lymphoblastoid B cell line established from a Burkitt lymphoma patient. Raji cells are widely used as a model for B-cell malignancies and immune response studies, retaining characteristics of mature B lymphocytes including antibody production capacity. Their transformed nature facilitates in vitro culture, while their signaling networks remain relevant for dissecting pathways involved in lymphomagenesis and immune cell function.
MAP2K4 encodes a dual-specificity MAP kinase kinase that integrates upstream stress and cytokine signals to activate the JNK and p38 pathways. It is activated by MAP3K family members (MEKK1, MLK3, ASK1, TAK1) in response to TNF-??, IL-1??, TGF-??, UV irradiation, and osmotic shock. Activated MAP2K4 phosphorylates JNK1/2/3 and p38 (MAPK14/11/12/13), which then phosphorylate transcription factors such as c-Jun, ATF2, and p53, thereby modulating AP-1 transcriptional activity. Scaffold proteins like JIP and ??-arrestin facilitate signal specificity.
In Raji B cells, MAP2K4-mediated JNK and p38 signaling is implicated in regulating apoptosis, proliferation, and inflammatory cytokine production. The knockout of MAP2K4 in this cell line is expected to disrupt these downstream pathways, potentially altering cell survival and stress responses relevant to Burkitt lymphoma pathology. Given the role of EBV transformation in modulating host signaling, this model enables dissection of viral and cellular kinase cascades that contribute to B-cell immortalization and tumorigenesis. Researchers can explore how loss of MAP2K4 impacts the interplay between oncogenic stress and apoptotic machinery in lymphoblastoid cells.
These polyclonal knockout cells enable B-cell signaling studies, lymphoma pathogenesis research, and drug target validation. Typical assays include Western blotting to confirm MAP2K4 loss and reduced JNK/p38 phosphorylation, RT-qPCR for AP-1 target genes, flow cytometry for apoptosis and cell cycle, and cytokine stimulation assays. Viability assays such as MTT/XTT assess stress responses. For further information, please contact Ascent Research.
