The MAPK9 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population of Raji B lymphocytes with targeted disruption of the MAPK9 gene, which encodes the stress-activated kinase JNK2. This loss-of-function model enables investigation of JNK2-dependent signaling without clonal selection bias. The polyclonal format ensures robust target-gene disruption while maintaining population-level heterogeneity, suitable for pooled screening and comparative pathway analyses.
Raji cells are a suspension-adapted Burkitt??s lymphoma-derived B lymphoblast line, positive for Epstein-Barr virus (EBV). These malignant B lymphocytes model germinal center B-cell biology and are leveraged in lymphoma research, apoptosis studies, and drug development. Their rapid proliferation and cytokine responsiveness facilitate high-throughput functional assays.
MAPK9 (JNK2) is a stress-activated mitogen-activated protein kinase phosphorylated by upstream kinases MKK4 and MKK7, which are activated by MAP3Ks including ASK1 and MEKK1 downstream of TNF receptor and Toll-like receptor stimulation. Once activated, JNK2 phosphorylates transcription factors such as c-Jun, ATF2, Elk-1, and NFATc4, promoting AP-1-mediated gene expression. Scaffold proteins JIP1, JIP2, and JIP3 organize the JNK signaling complex, while ??-arrestin-2 modulates JNK2 activation. Through these interactions, JNK2 integrates signals from TNF, IL-1, and TLRs to regulate apoptosis, proliferation, and differentiation, functioning as a central node in stress-responsive transcriptional programs.
In Raji B lymphocytes, JNK2 critically influences cell survival and apoptotic decisions. JNK signaling can mediate both pro- and anti-apoptotic outcomes, and MAPK9 knockout is anticipated to impair stress-induced apoptosis and alter chemosensitivity. This polyclonal knockout population provides a physiologically relevant system to dissect JNK2-specific contributions to oncogenic signaling, drug resistance, and immune mechanisms in Burkitt??s lymphoma, enabling comparative studies with parental Raji cells.
Applications include Western blotting for phospho-JNK, phospho-c-Jun, and downstream targets; apoptosis assays (Annexin V); proliferation and drug sensitivity testing (MTS); and JNK inhibitor screening. RT-qPCR and flow cytometry enable monitoring of transcriptional changes and B-cell marker expression. The polyclonal format supports population-based signaling studies and functional genomics in a lymphoblast context relevant to B-cell malignancies and immune disorders. For further details, contact Ascent Research.
