The CNNM3 Knockout Raji Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human Raji B lymphocyte cell line, engineered to disrupt the CNNM3 gene. This polyclonal pool offers a heterogeneous loss-of-function model for investigating CNNM3-mediated magnesium transport without clonal selection, preserving biological variability relevant to population-level studies. The cells are provided as a ready-to-use knockout resource for functional genomics and cell biology applications in immunology and cancer research.
The parental Raji cell line is an EBV-positive B lymphoblastoid line originally isolated from a Burkitt lymphoma patient. Raji cells grow in suspension and exhibit characteristic B cell features, including surface immunoglobulin expression, antigen presentation capacity, and the potential for differentiation into antibody-secreting cells under appropriate conditions. Widely employed in immunological investigations, Raji cells serve as a well-characterized model system for studying B lymphocyte biology, viral oncogenesis, and lymphomagenesis.
CNNM3 encodes a cyclin-related magnesium transporter that primarily facilitates magnesium efflux, thereby playing a critical role in intracellular magnesium homeostasis. The transporter functions within the TRPM7/TRPM6 magnesium transport pathway, where it is regulated by cellular magnesium levels and TRPM7 kinase activity. CNNM3 interacts with TRPM7 and cyclin-related motifs, and its activity influences downstream intracellular magnesium concentrations, which in turn modulate numerous magnesium-dependent cellular processes. Other pathway components include TRPM6, SLC41A1, and free magnesium ions. Through these interactions, CNNM3 helps maintain the delicate balance of this essential divalent cation, impacting enzyme activities, ion channel function, and metabolic signaling.
In the Raji B lymphocyte context, disruption of CNNM3 is anticipated to perturb magnesium homeostasis, potentially altering cellular proliferation, survival, and apoptosis. Given the established links between magnesium availability and tumor progression, this knockout model provides a valuable tool for dissecting the role of magnesium transporters in lymphoma biology. Moreover, because Raji cells are derived from a hematologic malignancy and are EBV-positive, the model may offer insights into how magnesium dysregulation collaborates with viral oncoproteins or affects immune cell function, including antigen presentation and differentiation pathways.
Typical applications include quantitative analysis of magnesium flux using fluorescent indicators such as Mag-Fura-2, flow cytometric measurement of intracellular magnesium levels, and cell proliferation or apoptosis assays to assess functional consequences of CNNM3 loss. The cells are suitable for Western blotting and RT-qPCR validation of knockout efficiency, as well as for ion channel/transporter functional studies and drug target validation campaigns in lymphoma and magnesium-related disorders. Their polyclonal nature supports population-based assays that demand biological replicates with inherent genetic heterogeneity. For further information, please contact Ascent Research.
