The LMF2 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Raji human B lymphoblastoid line, featuring targeted disruption of the LMF2 gene to create a stable loss-of-function model. This polyclonal format ensures robust representation of edited alleles while abolishing LMF2 protein expression, enabling bulk population studies of its cellular roles.
Raji cells originate from an EBV-positive Burkitt lymphoma patient and serve as a canonical model for B lymphocyte biology. They express characteristic markers CD19 and CD20, and their lymphoblastoid phenotype supports investigation of antigen presentation, signaling, and oncogenic processes. This background provides a physiologically relevant B cell context for exploring lipid metabolism and chaperone functions mediated by LMF2.
LMF2 encodes an ER-resident chaperone that specifically facilitates the folding and assembly of lipoprotein lipase (LPL) and hepatic lipase (HL). Functioning in concert with LMF1, LMF2 ensures productive maturation of these lipases, which are critical for hydrolyzing triglycerides carried by VLDL. LMF2 is transcriptionally regulated by PPAR?? and SREBP1c in response to nutrient signals. Knockout of LMF2 disrupts endoplasmic reticulum processing, leading to impaired secretion of active LPL and HL, reduced triglyceride hydrolysis, and subsequent lipid accumulation in cells.
In Raji B lymphocytes, the LMF2 knockout model enables examination of how lipid homeostasis influences immune cell function. B cells depend on fatty acid oxidation for energy during activation; defective lipase maturation may alter metabolic flux and impact proliferation or survival. This system is particularly relevant for modeling hypertriglyceridemia-associated immune dysfunction and combined lipase deficiency, shedding light on the intersection of ER chaperone biology and lymphocyte pathophysiology.
Researchers can leverage this polyclonal knockout product for detailed functional analyses, including Western blotting and RT-qPCR to confirm LMF2 disruption, lipoprotein lipase activity assays to quantify enzymatic output, and Oil Red O staining to visualize lipid droplet buildup. Flow cytometry for B cell surface antigens (CD19, CD20) assesses any phenotypic alterations. These assays support investigations into LMF2-dependent pathways in lipid metabolism and B cell biology. Contact Ascent Research for more information.
