The LTA4H Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population designed for loss-of-function studies of the LTA4H gene. The product consists of a heterogeneous pool of Raji cells subjected to CRISPR/Cas9-mediated gene disruption, ensuring a broadly applicable model without clonal biases. This polyclonal format provides a robust system for investigating the role of leukotriene A4 hydrolase in immune signaling and disease.
Raji cells are a well-characterized human Burkitt lymphoma line of B lymphocyte origin, positive for Epstein?CBarr virus and adapted to suspension culture. Widely employed in immunology and cancer research, Raji cells exhibit features of mature B cells, including surface immunoglobulin expression and competence for cytokine secretion, making them suitable for studying leukotriene-mediated pathways in a lymphoid context. Their EBV status also offers a unique platform for examining viral?Chost interactions in leukotriene signaling.
LTA4H encodes a bifunctional enzyme that catalyzes the hydrolysis of leukotriene A4 to the potent pro-inflammatory lipid mediator leukotriene B4. LTB4 signals through the G protein-coupled receptors BLT1 and BLT2, leading to activation of downstream effectors including PI3K/AKT and MAPK (ERK) pathways. The enzyme also possesses aminopeptidase activity. LTA4H expression is induced by upstream regulators such as NF-??B, inflammatory cytokines TNF-?? and IL-1??, and lipopolysaccharide. Its activity is closely linked to 5-lipoxygenase and the scaffold protein FLAP, which together orchestrate leukotriene biosynthesis.
In the Raji B-lymphocyte background, disruption of LTA4H abrogates LTB4 generation, thereby eliminating autocrine and paracrine LTB4 signaling through BLT1 and BLT2. This blockade is expected to dampen PI3K/AKT and ERK pathway activation, altering leukocyte chemotaxis, activation, and cytokine output. Given the role of LTB4 in amplifying inflammation, this knockout model is highly relevant for studying pathological processes such as asthma, atherosclerosis, and B-cell malignancies, where aberrant eicosanoid signaling contributes to disease progression.
Researchers can employ LTA4H Knockout Raji Polyclonal Cells to dissect leukotriene signaling networks, validate LTA4H inhibitors in drug sensitivity assays, and evaluate LTB4 secretion via ELISA. The model is suitable for chemotaxis assays, flow cytometric profiling of BLT receptor expression, and transcriptomic analyses by RNA-seq. It supports investigations into inflammation, lipid mediator biology, cancer immunology, and drug target validation. For further inquiries, please contact Ascent Research.
