The MAPK7 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from Raji B lymphocytes, featuring targeted disruption of the MAPK7 gene. This heterogeneous pool of knockout cells maintains the biological diversity of the original cell line while introducing loss-of-function mutations in ERK5, providing a versatile model for functional studies without the biases associated with single-cell cloning.
The Raji cell line is an Epstein-Barr virus (EBV)-positive human Burkitt??s lymphoma-derived lymphoblastoid B-cell line. Raji cells are widely employed as a model for lymphomagenesis and immune cell signaling due to their robust growth and well-characterized oncogenic pathways. This background offers a relevant system for investigating B-cell malignancies and virus?Chost interactions.
The MAPK7 gene encodes ERK5, a serine/threonine kinase central to the MAPK/ERK5 signaling cascade. ERK5 is activated primarily through dual phosphorylation by MEK5 (MAP2K5) following stimulation by growth factors such as EGF, oxidative stress, or cytokines including IL-6, with upstream regulation by MEKK2/3 (MAP3K2/3). Upon activation, ERK5 translocates to the nucleus and phosphorylates transcription factors MEF2C, MEF2D, and c-Myc, as well as c-Fos and Sap1a, to promote gene expression programs governing cell proliferation, survival, differentiation, and angiogenesis. ERK5 also interacts with scaffold proteins 14-3-3 and IQGAP1, and crosstalks with the PI3K-Akt pathway, collectively modulating cellular senescence and stress responses.
In Raji B-lymphoma cells, ERK5 signaling contributes to the malignant phenotype by sustaining proliferation and inhibiting apoptosis. Disruption of MAPK7 in this polyclonal knockout population enables dissection of ERK5-dependent oncogenic mechanisms, including the transcriptional regulation of c-Myc, a key driver in Burkitt??s lymphoma pathogenesis. Researchers can use the model to assess how ERK5 loss impacts growth factor responsiveness, angiogenic factor production, and cellular stress adaptation within an EBV-positive B-cell context, providing insights into lymphoma biology and potential therapeutic vulnerabilities.
Experimental applications include Western blotting to detect total and phosphorylated ERK5, RT-qPCR for quantifying downstream targets MEF2C and c-Myc, flow cytometry for cell cycle and apoptosis analyses, and MTT proliferation assays. The polyclonal knockout cells are also well-suited for kinase inhibitor screening, allowing assessment of ERK5-targeted compounds in a lymphoma-relevant system. For additional product information or technical support, please contact Ascent Research.
