The CSNK2A1 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population offering a loss-of-function model for the CSNK2A1 gene in human Raji B lymphocytes. This product provides a heterogeneous pool of edited cells, each carrying target-gene disruption via CRISPR/Cas9-mediated genome editing, enabling robust functional interrogation without clonal selection artifacts.
The host Raji cell line is derived from an Epstein-Barr virus (EBV)-transformed Burkitt lymphoma patient and grows in suspension, retaining immunoglobulin secretion capability. As a well-established model for Burkitt lymphoma and other B-cell malignancies, Raji cells exhibit constitutive activation of survival pathways driven in part by aberrant CK2 kinase activity, making them an ideal background for CSNK2A1 knockout studies.
CSNK2A1 encodes the catalytic ?? subunit of the serine/threonine kinase CK2, which phosphorylates a vast array of substrates involved in cell cycle progression, apoptosis suppression, DNA repair, and signal transduction. CK2 holoenzyme, often composed of two CSNK2A1 and two CSNK2B regulatory subunits, mediates pro-survival signaling downstream of growth factors and cellular stress, with upstream regulators including interleukin-6 and tumor necrosis factor alpha. Key downstream targets include AKT1, ??-catenin (CTNNB1), NF-??B p65 (RELA), PTEN, TP53, CDC25A, MCL1, and BIRC5 (survivin). The kinase also interacts with PIN1, HSP90, and importins to modulate substrate accessibility and nuclear translocation. CSNK2A1 knockout eliminates CK2 catalytic function, leading to abrogated phosphorylation of these targets and subsequent disruption of PI3K/AKT, Wnt/??-catenin, and NF-??B signaling cascades.
In the Raji cell context, CK2 overexpression contributes to oncogenic transformation and resistance to apoptosis. Disruption of CSNK2A1 dismantles this kinase-dependent survival network, thereby sensitizing cells to intrinsic and extrinsic apoptotic stimuli. This knockout model recapitulates the loss of CK2 activity and provides a physiologically relevant platform to dissect CK2-driven signaling in B-cell lymphoma, including the interplay with DNA damage response pathways and the BCL2 family-regulated apoptosis machinery.
Typical applications include functional studies of CK2 in B-cell malignancies, validation of small-molecule CK2 inhibitors such as CX-4945, interrogation of apoptosis resistance mechanisms, and dissection of oncogenic signaling networks. Researchers can employ this knockout model in a range of assays: Western blotting for phospho-AKT and phospho-??-catenin to assess pathway activity, flow cytometry-based Annexin V/7-AAD apoptosis measurement, MTS or CellTiter-Glo proliferation assays, and RNA-seq transcriptomic profiling. Co-immunoprecipitation of CK2 substrates and caspase activity assays further enable mechanistic exploration, while drug sensitivity testing with CK2 inhibitors supports translational research. For additional information on this product, please contact Ascent Research.
