The LYRM1 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population disrupting the LYRM1 gene in human Raji B lymphocytes. This loss-of-function model enables investigation of LYRM1??s role in mitochondrial iron-sulfur cluster assembly, respiratory complex I function, and energy metabolism. The polyclonal format maintains genetic heterogeneity, avoiding clonal selection biases, and allows robust functional analyses of LYRM1 ablation consequences.
The Raji cell line, originating from EBV-positive Burkitt lymphoma, serves as a model of human B lymphocytes with antibody production and immune response capabilities. Its malignant origin and viral status make it ideal for studying lymphomagenesis, immune cell metabolism, and viral?Cmitochondrial interactions. Raji cells provide a reproducible, well-characterized background for dissecting gene function in B cell contexts.
LYRM1 is a mitochondrial Fe-S cluster assembly factor that interacts with LYRM4, NDUFAF1, ISCU, and frataxin (FXN). It is regulated by PPARG, NRF1, and PPARGC1A, linking adipogenic and oxidative programs. LYRM1 supports complex I maturation by influencing NDUFS1, ND4, and UQCRB, and affects fatty acid oxidation via ACADM. Its disruption impairs Fe-S transfer, reduces complex I activity, and diminishes oxidative phosphorylation, placing LYRM1 at a nexus of mitochondrial biogenesis and lipid metabolism.
In Raji cells, LYRM1 knockout likely compromises mitochondrial Fe-S supply, attenuates complex I, and alters bioenergetics. Burkitt lymphoma cells depend on both oxidative phosphorylation and glycolysis; thus, metabolic dependency may shift, impacting proliferation. Additionally, LYRM1??s adipogenic regulation suggests its loss could dysregulate lipid metabolism, modeling metabolic reprogramming in lymphoma and providing insights into mitochondrial dysfunction?Concogenesis crosstalk in an EBV-positive B cell environment.
These polyclonal knockout cells support assays such as Western blot, RT-qPCR, Seahorse flux analysis, MitoTracker staining, flow cytometry for apoptosis, and complex I activity assays. They are suited for research into mitochondrial dysfunction, adipogenesis, obesity, type 2 diabetes, and metabolic rewiring in B cell lymphoma. Investigators exploring Fe-S cluster biology, respiratory chain defects, or lymphoma metabolism will benefit from this model. For further information, contact Ascent Research.
