The NAAA Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human Burkitt lymphoma Raji B lymphocyte line, with disruption of the NAAA gene. This mixed population harbors loss-of-function mutations generated by CRISPR/Cas9-mediated gene editing. NAAA encodes N-acylethanolamine acid amidase, a lysosomal enzyme hydrolyzing bioactive N-acylethanolamines such as palmitoylethanolamide (PEA). This knockout model is a valuable tool for studying endocannabinoid biology, lysosomal lipid metabolism, and related pathways in B lymphocytes.
The Raji host line is a human B lymphocyte line from a Burkitt lymphoma patient, positive for Epstein-Barr virus (EBV). Raji cells are widely used to model B cell functions including antibody production and antigen presentation. Their transformed phenotype and robust suspension growth suit diverse biochemical and pharmacological assays. The EBV-positive background also makes them relevant to viral host-interaction studies intersecting with lipid signaling and lysosomal function.
NAAA is a lysosomal hydrolase that cleaves N-acylethanolamines into fatty acids and ethanolamine, with PEA as a primary substrate. PEA activates peroxisome proliferator-activated receptor alpha (PPAR-??) to exert anti-inflammatory and analgesic effects. NAAA activity is regulated by lysosomal pH and the transcription factor TFEB, which drives lysosomal biogenesis. NAAA-mediated hydrolysis reduces PEA levels, attenuating PPAR-?? signaling and modulating inflammatory mediators. The enzyme interacts with lysosomal lipid transfer proteins and saposins. Fatty acid amide hydrolase (FAAH) provides an alternative N-acylethanolamine degradation route at the endoplasmic reticulum. Knockout of NAAA blocks this catabolism, causing PEA accumulation and sustained PPAR-?? activation, while reducing ethanolamine and fatty acid outputs.
In Raji B cells, NAAA knockout enables dissection of crosstalk between endocannabinoid/NAE signaling and immune function. The EBV-positive B cell background allows study of how enhanced PPAR-?? activation influences B cell proliferation, apoptosis, and antigen presentation. Accumulated PEA mimics pharmacological NAAA inhibition, offering insights into therapies for inflammation, pain, and cancer. Given the lymphoma origin, this model also supports investigation of lipid-mediated regulation of tumorigenesis and immune evasion.
This polyclonal knockout population suits mechanistic studies of lysosomal lipid metabolism, NAAA inhibitor screening, and biomarker discovery for N-acylethanolamine-related disorders. Assays include Western blot and RT-qPCR for NAAA validation, LC-MS for PEA quantitation, and flow cytometry for inflammatory markers. Functional analyses can use apoptosis and cytokine release assays alongside NAAA inhibitor treatments. Lipidomic profiling can reveal broader metabolic changes. Researchers in endocannabinoid biology, inflammation, pain, neurodegeneration, or metabolic syndromes will find these cells a robust loss-of-function model. For technical details or ordering, contact Ascent Research.
