The CD320 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from Raji B lymphocytes, with targeted disruption of the CD320 gene. This loss-of-function model enables investigation of the transcobalamin receptor’s role in vitamin B12 uptake and related metabolic pathways.
Raji cells, a human B lymphoblastoid line from Burkitt lymphoma, are EBV-positive and widely used in immunological and cancer research. They exhibit antibody production, antigen presentation, and immune surveillance functions, making them ideal for studying B cell biology and lymphoma metabolic dependencies.
The CD320 gene encodes the receptor for transcobalamin-bound cobalamin (vitamin B12), mediating cellular uptake of this micronutrient. Upon binding the holo-TCN2 complex, CD320 internalizes cobalamin, which then serves as a cofactor for methionine synthase (MTR) and methylmalonyl-CoA mutase (MUT). These enzymes are pivotal in the methionine cycle and one-carbon metabolism, driving DNA methylation, nucleotide synthesis, and cell proliferation. CD320 activity is modulated by cellular cobalamin levels and growth factor signaling. Disruption of CD320 blocks B12 import, leading to impaired MTR and MUT function, reduced S-adenosylmethionine (SAM) production, and consequent metabolic dysregulation.
In Raji B lymphoblastoid cells, CD320 knockout provides a system to explore the link between vitamin B12 metabolism and oncogenic processes. The high proliferation rate of Burkitt lymphoma may depend on one-carbon metabolism, revealing metabolic vulnerabilities. Loss of CD320-driven B12 uptake can illuminate how methyl group availability impacts epigenetic regulation, nucleotide biosynthesis, and cell survival, offering insights into therapeutic targets in lymphoma.
Research applications include studies of B12 trafficking in B cells, identification of metabolic checkpoints in lymphoma, and screening of B12 transport inhibitors. Compatible assays include vitamin B12 uptake, cell viability (MTT), proliferation (BrdU), apoptosis (Annexin V), western blot for MTR, metabolomics, and methionine synthase activity assays. For further details, please contact Ascent Research.
