The MAPK10 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population engineered to disrupt the MAPK10 gene in the human Raji B lymphocyte line. This polyclonal format provides a genetically diverse pool for functional analysis of JNK3 (MAPK10), enabling robust evaluation of gene disruption effects across a mixed cellular background.
Raji cells are an EBV-positive B lymphocyte line derived from a Burkitt’s lymphoma patient. They serve as a well-characterized model for B-cell biology, humoral immunity, and lymphomagenesis, supporting studies of antigen presentation, antibody production, and Epstein-Barr virus latency.
MAPK10 encodes JNK3, a stress-activated serine/threonine kinase that functions as the terminal member of the c-Jun N-terminal kinase cascade. JNK3 is predominantly activated by phosphorylation through MKK4 and MKK7, which are themselves regulated by upstream MAP3Ks including ASK1, MEKK1, and TAK1 in response to stimuli such as TNFR1 engagement, B cell receptor (BCR) ligation, and Toll-like receptor 4 (TLR4) activation. Once phosphorylated, JNK3 translocates to the nucleus and phosphorylates transcription factors c-Jun, ATF2, and JunD, thereby modulating AP-1-dependent gene expression. Signaling specificity is enforced by scaffold proteins JIP1, JIP2, and JIP3, while negative regulation is mediated by the phosphatase MKP5, positioning JNK3 at a critical node controlling apoptosis, inflammation, and cellular stress responses.
In Raji B cells, JNK3 integrates extracellular signals from the BCR complex, CD40, and TLR4 to influence transcriptional programs governing proliferation, survival, and EBV latency. MAPK10 knockout in this context provides a loss-of-function model to dissect how JNK3 activity contributes to EBV-mediated oncogenesis, BCR-driven survival pathways, and the balance between latent and lytic viral states. This model is particularly relevant for elucidating signaling networks that sustain lymphoma cell viability and for identifying therapeutic vulnerabilities in B-cell lymphomas.
Typical applications include investigation of JNK3 function in BCR and TLR signaling cascades using phospho-kinase arrays and AP-1 luciferase reporter assays. Apoptosis and stress responses can be assessed via flow cytometric Annexin V/PI staining, while co-immunoprecipitation enables analysis of JNK3 signaling complexes. These polyclonal cells are also suitable for RT-qPCR and Western blotting for total and phosphorylated JNK3, as well as drug sensitivity assays to evaluate JNK3 inhibitors. For further information or to request a quote, please contact Ascent Research.
