The ACBD5 Knockout Jurkat Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population generated from the Jurkat human T lymphocyte line. This pooled population carries targeted disruptions in the ACBD5 gene, offering a loss-of-function model for investigating peroxisomal biology in an immune cell context. Designed for researchers studying lipid metabolism and T cell signaling, these cells provide a heterogeneous knockout platform for functional genomics and metabolic studies.
Jurkat cells are an immortalized T lymphocyte line derived from a patient with acute T cell leukemia, and they serve as a canonical system for dissecting T cell receptor (TCR) signaling, apoptosis, and immune activation pathways. Their sustained proliferation and well-characterized signaling networks make them an ideal host for examining the consequences of metabolic gene disruptions, such as ACBD5 knockout, on T cell physiology.
ACBD5 functions as an acyl-CoA binding protein that facilitates the peroxisomal import and beta-oxidation of very-long-chain fatty acids. It interacts with the peroxisomal biogenesis factors PEX19 and PEX5, and partners with ABCD1 to mediate substrate translocation. ACBD5 is transcriptionally regulated by PPAR alpha and is responsive to insulin signaling, linking its expression to systemic and cellular lipid metabolic states. Disruption of ACBD5 abrogates efficient very-long-chain fatty acid degradation, resulting in lipid accumulation and peroxisomal stress that can perturb downstream metabolic and signaling networks.
In the Jurkat T cell environment, ACBD5 knockout allows exploration of how peroxisomal lipid handling impacts T cell functions, including metabolic adaptation during activation. Since T cells rely on fatty acid oxidation for energy and membrane biosynthesis, impaired peroxisomal beta-oxidation may modulate TCR signal strength, cytokine production, or apoptotic thresholds. This model is therefore valuable for studying peroxisomal disorders and immune-metabolic cross-talk relevant to neuroinflammation and other conditions.
Researchers can utilize these polyclonal cells for Western blotting of ACBD5 and peroxisomal markers, RT-qPCR profiling of peroxisomal genes, and liquid chromatography?Cmass spectrometry quantification of very-long-chain fatty acids. Functional readouts include flow cytometric analysis of cell cycle and apoptosis, immunofluorescence microscopy for peroxisome morphology, and phospho-signaling assessment of TCR activation cascades. This system supports drug screening and mechanistic studies targeting peroxisomal pathways in immune cells. For further details, contact Ascent Research.
