MAP3K21 Knockout Raji Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human Raji B lymphocyte cell line. This product disrupts the MAP3K21 gene encoding a serine/threonine kinase of the mixed lineage kinase subfamily. The polyclonal population provides a heterogeneous loss-of-function model for investigating kinase-dependent signaling networks, free from clonal bias. Researchers can employ these cells to study MAP3K21-mediated signal transduction in a B-cell lymphoma context using standard gene editing technology.
The parental Raji cell line originates from a Burkitt’s lymphoma patient and is Epstein-Barr virus (EBV)-positive, grows in suspension, and retains B lymphocyte characteristics. It serves as a well-established model for B-cell malignancies and EBV-driven oncogenesis, making it an ideal host for examining the role of MAP3K21 in lymphoma biology.
MAP3K21 functions upstream of the JNK and p38 MAPK cascades, responding to stimuli such as TNF-??, IL-1, Toll-like receptor ligands, and oxidative stress. Activated by TRAF2 and RIPK1, MAP3K21 phosphorylates MKK4 and MKK7, which then activate JNK1/2/3. Alternatively, it signals via MKK3/6 to p38 MAPK. Phosphorylated JNK translocates to the nucleus and targets transcription factors c-Jun and ATF2, modulating gene expression linked to apoptosis and proliferation. Scaffold proteins JIP and 14-3-3 regulate MAP3K21 signaling complexes.
In Raji B cells, MAP3K21-mediated signaling may influence EBV-associated oncogenic processes, cell survival, and response to therapeutic stress. Disruption of MAP3K21 enables investigation into how this kinase contributes to cytokine responsiveness, stress-induced apoptosis, and the maintenance of the malignant state in Burkitt’s lymphoma, highlighting vulnerabilities for targeted intervention.
Typical assays include western blotting for MAP3K21 and phospho-JNK, Annexin V/PI apoptosis flow cytometry, MTS proliferation assays, and phospho-kinase arrays. Transcriptional outputs can be measured by RT-qPCR or AP-1 luciferase reporter assays, while protein interactions are probed by co-immunoprecipitation. These tools facilitate research into JNK signaling in B-cell lymphomas, identification of lymphoma drug targets, and elucidation of EBV?Chost interactions. For further details and ordering, contact Ascent Research.
