The FAAH2 Knockout Raji Polyclonal Cells product provides a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Raji human B lymphocyte line, designed to disrupt the FAAH2 gene. This loss-of-function model enables investigation of FAAH2-dependent biological processes without the artifacts that can arise in clonal isolates. As a polyclonal pool, the product offers a heterogeneous background that averages out potential off-target or site-specific effects, making it suitable for bulk biochemical, lipidomic, and functional studies where population-level responses are of primary interest.
The Raji cell line originates from an Epstein-Barr virus (EBV)-positive human Burkitt’s lymphoma and serves as a widely used model for B-cell biology, immune signaling, and oncogenic transformation. These suspension-adapted lymphoblastoid cells maintain robust antigen presentation machinery and are capable of antibody production, while constitutively active NF-??B and latent EBV gene expression programs create a unique cellular environment for studying signaling crosstalk. Their high transfection efficiency and reproducible growth characteristics make them amenable to genetic editing and downstream assay workflows.
FAAH2 encodes a serine hydrolase that hydrolyzes primary fatty acid amides, most notably oleamide, thereby terminating their lipid signaling functions. Disruption of FAAH2 leads to accumulation of these bioactive lipids, which can engage cannabinoid receptors CB1 and CB2, activate peroxisome proliferator-activated receptor alpha (PPAR-alpha), and modulate NF-??B transcriptional programs. Upstream regulators of FAAH2 include androgen receptor signaling and endoplasmic reticulum (ER) stress, while the enzyme itself interacts with membrane lipids, ER-resident proteins, and fatty acid binding proteins, situating it at a key intersection of lipid metabolism and intracellular signaling networks.
In the Raji B lymphocyte context, FAAH2 knockout allows dissection of how fatty acid amide catabolism influences immune cell functions such as antibody secretion, antigen presentation, and proliferation. The constitutive NF-??B activity inherent in Raji cells provides a baseline against which FAAH2-dependent modulation can be measured, offering insights into how endocannabinoid-related lipid signals intersect with oncogenic and inflammatory pathways. This is particularly relevant for prostate and breast cancer research, where aberrant lipid signaling and immune cell interactions are increasingly recognized.
Researchers can employ this knockout model in dose-response analyses with cannabinoid receptor ligands, siRNA rescue experiments, and drug target validation screens. Representative assays include Western blotting for FAAH2 protein, fluorogenic enzyme activity measurements, and LC-MS/MS lipidomics for oleamide quantification. Functional outcomes such as apoptosis by flow cytometry and cell proliferation are readily assessed. This model supports research in endocannabinoid biology, inflammation, and oncology. For further information, please contact Ascent Research.
