The FABP4 Knockout Raji Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Raji B lymphocyte line. This product offers a loss-of-function model for studying fatty acid-binding protein 4 (FABP4) in a human B cell context. The polyclonal format provides a heterogeneous pool of edited cells, each carrying distinct gene-disruption events, enabling robust assessment of FABP4 depletion effects across a population.
Raji cells are an Epstein-Barr virus (EBV)-positive Burkitt??s lymphoma-derived B lymphoblastoid line, widely employed as a model for malignant B cell studies and immune signaling. The EBV-transformed phenotype confers continuous proliferation and expression of B cell surface markers, making these cells suitable for investigating lipid metabolism and inflammatory pathways in a B cell lineage.
FABP4 functions as an intracellular lipid chaperone governing fatty acid availability for metabolism and signaling. It directly interacts with lipid droplets and hormone-sensitive lipase (HSL), regulating lipolysis and fatty acid efflux. FABP4 also facilitates nuclear targeting of PPAR??, which controls genes like CD36 and lipoprotein lipase (LPL). Induced by PPAR??, C/EBP??, LXR, insulin, and cytokines TNF-?? and IL-4, FABP4 is suppressed by glucocorticoids. FABP4 modulates NF-??B and JNK cascades via arachidonic acid and prostaglandin precursors, with IKK?? and JNK as downstream kinases. Knockout disrupts these interactions, impairing PPAR??-mediated transcription and blunting NF-??B/JNK inflammatory responses.
Disruption of FABP4 in Raji B lymphocytes eliminates the lipid chaperone essential for intracellular fatty acid trafficking and PPAR??-mediated gene regulation. In these malignant B cells, the loss of FABP4 impairs the utilization of exogenous fatty acids and the production of lipid mediators, leading to diminished NF-??B and JNK signaling. Consequently, the polyclonal knockout population displays reduced secretion of inflammatory cytokines and altered metabolic flux, providing a direct link between lipid handling and immune signaling in a B cell lymphoma context. The EBV-driven background further highlights the interplay between viral transformation and lipid-dependent inflammatory pathways, making this model valuable for dissecting metabolic vulnerabilities in lymphomagenesis.
This FABP4 knockout polyclonal model is suited for a wide range of research applications, including metabolic disease and inflammation studies, where it can be used to assess cytokine secretion by ELISA, fatty acid uptake and lipid droplet staining, and NF-??B or PPAR?? reporter activity. The polyclonal population is also applicable in lymphoma-focused cancer metabolism studies, enabling drug sensitivity profiling against chemotherapeutic agents and metabolic flux analyses. Transcriptomic profiling via RNA-seq can uncover global changes in lipid signaling networks, while Western blotting and RT-qPCR allow confirmation of FABP4 protein and mRNA knockdown. For further information or technical support, please contact Ascent Research.
