The PEA15 Knockout Raji Polyclonal Cells are produced by CRISPR/Cas9-mediated gene disruption in the Raji B lymphocyte host, yielding a polyclonal knockout cell population with diverse PEA15 mutations. This format avoids clonal selection, providing a more representative model for studying gene function in a heterogeneous cellular context. The product is intended for advanced apoptosis and MAPK pathway investigations.
The Raji cell line is an EBV-positive B lymphocyte model derived from Burkitt??s lymphoma, growing in suspension. It is widely used for research into immune cell biology, antibody production, and antigen presentation. The EBV-driven background promotes dysregulated growth and survival signaling, making it a valuable system for studying lymphomagenesis and B-cell receptor pathways. Raji cells exhibit hallmark features of aggressive B-cell malignancy, facilitating the exploration of oncogenic mechanisms and therapeutic vulnerabilities.
PEA15 is a scaffold protein integrating MAPK/ERK and death receptor signals to control apoptosis, proliferation, and glucose metabolism. Upstream kinases CaMKII, PKC, and Akt, along with TNF-alpha and EGF, phosphorylate PEA15, modulating its interactions. PEA15 binds and retains ERK1/2 in the cytoplasm, blocking nuclear translocation and Elk-1 transactivation. Separately, it interacts with FADD and Caspase-8 to inhibit death-inducing signaling complex assembly, suppressing extrinsic apoptosis. Associated factors include RSK, PLD1, and Importin, linking PEA15 to transport and phospholipid signaling. Thus, PEA15 serves as a switch balancing survival versus death via ERK/RSK and caspase cascades.
In the Raji B-cell lymphoma context, PEA15 knockout likely alters the balance between ERK-driven proliferation and death receptor-mediated apoptosis. As Burkitt??s lymphoma cells often display elevated MAPK activity, loss of PEA15-mediated ERK1/2 cytoplasmic sequestration may enhance nuclear signaling and cell cycle progression. Conversely, abrogation of FADD binding could sensitize cells to extrinsic apoptotic stimuli, enabling dissection of resistance to TRAIL or FAS ligand. This model provides insight into B-cell malignancy mechanisms and has relevance for glioblastoma, breast cancer, and metabolic or neurodegenerative disorders linked to PEA15.
Researchers can use these cells in apoptosis and MAPK signaling assays, including Western blotting of phospho-ERK1/2, RT-qPCR of pathway targets, and flow cytometry-based apoptosis detection (e.g., Annexin V/PI). Cell viability and colony formation assays support proliferation studies, while co-immunoprecipitation and immunofluorescence enable analysis of PEA15 complexes and localization. This polyclonal knockout model is suited for B-cell lymphoma drug screening and cancer cell proliferation experiments. For further details, contact Ascent Research.
