The DBI Knockout Raji Polyclonal Cells product is a CRISPR/Cas9-edited polyclonal knockout cell population generated from the human Raji B lymphocyte line. This model carries targeted disruption of the DBI gene, which encodes the acyl-CoA binding protein (ACBP, also referred to as diazepam binding inhibitor). The polyclonal format yields a diverse pool of cells harboring various loss-of-function mutations, enabling robust population-level analyses without clonal selection. It serves as a versatile tool for studying DBI deficiency in a well-characterized Burkitt lymphoma-derived B-cell background.
The Raji host cell line is a classic human B-cell model derived from a Burkitt lymphoma patient. These cells exhibit key B-cell functions, including efficient antibody secretion and antigen presentation, and are extensively used in immunology, oncology, and metabolic research. Raji cells offer a reproducible and physiologically relevant system for examining gene function, signal transduction, and drug responses in a lymphoid context. Their stable growth and well-annotated biology ensure consistent experimental outcomes for gene-editing studies.
DBI/ACBP operates as an intracellular carrier of medium-chain acyl-CoA esters and as an allosteric regulator of the GABA-A receptor. Its transcription is controlled by the lipid-sensing factors SREBP1 and PPAR??, integrating metabolic status with gene expression. Through physical interaction with medium-chain acyl-CoA and the GABA-A receptor complex, DBI modulates acyl-CoA-dependent enzymatic activities and GABAergic neurotransmission. Downstream, it influences the GABA-A receptor’s function and enzymes that utilize acyl-CoA substrates, thereby connecting fatty acid metabolism, steroidogenesis, and neural signaling pathways.
In the Raji B-cell setting, DBI knockout is anticipated to compromise acyl-CoA transport, leading to disrupted intracellular lipid distribution and altered metabolic homeostasis. Since fatty acid metabolism is increasingly recognized as critical for B-cell activation, differentiation, and malignant transformation, this model permits dissection of how DBI-mediated lipid handling impacts antibody production, antigen presentation, and proliferative capacity. Additionally, if Raji cells express functional GABA-A receptor subunits, the knockout could perturb receptor-mediated signaling, enabling exploration of non-neuronal GABAergic functions.
This DBI knockout polyclonal cell model supports diverse research applications, including mechanistic studies of lipid metabolism?CGABAergic crosstalk, high-throughput screening for molecules that modulate DBI?CGABA-A receptor interaction, and functional analysis of DBI in B-cell biology and lymphomagenesis. Validated assay formats include western blotting, RT-qPCR, acyl-CoA binding assays, lipidomics, GABA-A receptor electrophysiology, and flow cytometry, providing comprehensive tools for molecular and functional characterization. For additional technical support and ordering information, please contact Ascent Research.
