The MAP2K7 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population, in which the MAP2K7 gene has been disrupted within the Raji B lymphoblast cell line. This product provides a heterogeneous pool of MAP2K7-deficient Raji cells, enabling loss-of-function studies of the MAP2K7 kinase across the polyclonal population without clonal isolation.
The Raji cell line is a suspension lymphoblast line established from a Burkitt??s lymphoma patient. As a model B lymphocyte line, Raji cells are widely employed to investigate B-cell receptor signaling, apoptosis regulation, and immune response mechanisms. Their lymphoblastoid origin and robust growth in suspension make them suitable for high-throughput immunological assays and cancer biology research.
MAP2K7 (MKK7) is a dual-specificity protein kinase that specifically phosphorylates and activates JNKs (MAPK8, MAPK9, MAPK10) in response to stress, cytokines, and developmental signals. Upstream MAP3Ks including TAK1 (MAP3K7), ASK1 (MAP3K5), and MEKK1 (MAP3K1) activate MAP2K7, often downstream of receptors such as TNFR1, IL-1R, TLRs, and CD40. Activated MAP2K7 dually phosphorylates JNK, which then translocates to the nucleus to phosphorylate transcription factors c-Jun and ATF2, thereby regulating AP-1-mediated gene expression. The activity of MAP2K7 is modulated by interactions with JIP scaffold proteins (JIP1/2/3), ??-arrestin, GADD45, and AXIN, which ensure signal fidelity and subcellular localization.
In the Raji B-lymphoma context, disruption of MAP2K7 abrogates a critical branch of JNK signaling, enabling dissection of the kinase??s role in lymphocyte activation, cytokine responses, and apoptosis. This polyclonal knockout model allows assessment of how JNK-dependent transcription affects proliferation, survival, and inflammatory mediator production in B-lymphoid cells. It is particularly valuable for studying Burkitt??s lymphoma biology and for testing JNK pathway inhibitors in hematological malignancies.
Researchers can employ this model in immunoblotting for phospho-JNK, AP-1 reporter assays, flow cytometric detection of phosphorylated c-Jun, and apoptosis profiling with Annexin V staining. RT-qPCR of JNK target genes and cytokine release assays provide further functional readouts, while drug sensitivity testing with JNK inhibitors and synthetic lethality screens are possible in the B-cell lymphoma setting. This tool helps advance understanding of JNK-mediated pathology in cancer, inflammation, and autoimmune disorders. For additional information or technical support, please contact Ascent Research.
