The MAP4K2 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population of the Raji human B lymphocyte line, engineered for loss-of-function studies of the MAP4K2 gene. This polyclonal format, rather than a clonal derivative, maintains biological heterogeneity and avoids artifacts of single-cell cloning, providing a robust model for investigating signaling events at the population level in immunological and oncological research contexts.
Raji is an Epstein-Barr virus (EBV)-positive Burkitt lymphoma B cell line originating from a mature B lymphocyte. It expresses surface immunoglobulin (BCR), co-stimulatory receptors, and antigen-presentation components, making it highly responsive to BCR ligation and cytokine stimulation. Because of its transformed phenotype and ease of culture, Raji is a well-established system for biochemical analyses and high-throughput screens in B cell malignancy and immune signaling studies.
MAP4K2 (also known as germinal center kinase, GCK) is a Ste20 family serine/threonine kinase that serves as an upstream activator of the JNK and p38 MAPK pathways. In response to BCR engagement, TNF??, CD40 ligand, oxidative stress, or IL-1??, MAP4K2 phosphorylates MAP3K1 (MEKK1). MEKK1 then activates MAP2K4/MAP2K7 to stimulate JNK1/2, and MAP2K3/MAP2K6 to stimulate p38 MAPK, culminating in phosphorylation of transcription factors c-Jun and ATF2 that regulate proliferation, survival, and apoptosis. MAP4K2 interacts with adaptor proteins TRAF2, TRAF6, BLNK (SLP-65), and GRB2, integrating it into proximal BCR and inflammatory receptor complexes.
In Raji B lymphocytes, MAP4K2 plays a critical role in coupling BCR and stress signals to MAPK cascades that control cell fate. Disrupting MAP4K2 in these polyclonal cells allows researchers to dissect the kinase’s contribution to lymphoma cell survival and apoptosis, and to investigate its involvement in B cell receptor?Cdependent survival pathways. The model is particularly suited for examining how dysregulation of the MAP4K2?CMEKK1?CJNK/p38 axis contributes to B lymphomagenesis. Additionally, because MAP4K2 associates with TRAF2/TRAF6, the knockout may uncover cross-talk between stress-activated MAPK pathways and NF-??B signaling.
Typical applications include anti-IgM or anti-CD40 stimulation coupled with phospho-JNK/p38 Western blotting, inhibitor screening to identify selective MAP4K2 blockers, and Annexin V?Cbased apoptosis assays following BCR or stress challenges. Cell proliferation can be measured by CFSE or BrdU, and MAP4K2 interactomes can be mapped via co-immunoprecipitation with TRAF2, TRAF6, or BLNK. RT-qPCR and phospho-kinase arrays enable downstream transcriptional and pathway profiling. These cells support functional genomics in B cell lymphoma, kinase drug discovery, and mechanistic studies of immune signal transduction. For further details, please contact Ascent Research.
