The HDLBP knockout Jurkat polyclonal cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Jurkat human T-lymphocyte cell line, in which the gene encoding HDLBP (high-density lipoprotein-binding protein, also known as vigilin) has been disrupted. This polyclonal knockout product, designated HDLBP Knouckout Jurkat Polyclonal Cells, provides a heterogeneous pool of cells with targeted gene disruption, enabling loss-of-function studies without the selection of a single clonal isolate. The use of CRISPR/Cas9-mediated gene disruption ensures efficient ablation of HDLBP expression across the population, offering a robust model for investigating the role of this RNA-binding protein in cholesterol metabolism and post-transcriptional gene regulation within a T-cell context.
The host Jurkat cell line is an immortalized T-lymphocyte line originally established from the peripheral blood of a 14-year-old acute T-cell leukemia patient. Jurkat cells are widely employed as a model system for studying T-cell receptor signaling, activation, apoptosis, and leukemia biology. Their suspension growth characteristics and well-characterized signaling pathways make them particularly suitable for investigating the intersection of lipid metabolism and immune cell function. As a CD4+ T-cell model, Jurkat cells retain many features of primary T-lymphocytes, including the ability to respond to various stimuli, providing a physiologically relevant background for examining hematopoietic cell signaling and lipid-dependent regulatory mechanisms.
HDLBP, or vigilin, is a 150 kDa RNA-binding protein containing multiple KH domains that mediate its interaction with high-density lipoproteins (HDL) and RNA. It functions as a key regulator of cellular cholesterol homeostasis by binding HDL particles via apolipoprotein A-I (apoA-I) and facilitating cholesterol efflux, while also modulating the stability and translation of mRNAs involved in lipid metabolism, such as PTEN and apoB. The activity of HDLBP is subject to regulation by upstream factors including the sterol regulatory element-binding protein 2 (SREBP2) and fluctuating cellular cholesterol levels. Downstream, HDLBP influences the expression of critical targets and participates in pathways involving ATP-binding cassette transporter A1 (ABCA1) and the low-density lipoprotein receptor (LDLR), thereby integrating cholesterol trafficking with post-transcriptional gene regulation.
In the Jurkat T-cell background, disruption of HDLBP function is predicted to impair cholesterol transport and the post-transcriptional control of genes essential for cell growth and signaling. Given that T-cell activation and function are influenced by membrane lipid composition and cholesterol availability, the loss of HDLBP is expected to perturb lipid rafts and signaling platforms, potentially affecting T-cell receptor-mediated pathways. Consequently, this knockout model serves as a valuable tool for dissecting the role of cholesterol metabolism in leukemic T-cell biology, including how alterations in HDL binding and RNA regulation impact immune cell signaling, proliferation, and apoptosis in a disease-relevant cellular environment.
The HDLBP knockout Jurkat polyclonal cells are suitable for a diverse range of experimental applications, including the study of cholesterol metabolism in T-cells, investigation of HDLBP function in immune cell signaling, host factor research for hepatitis C virus infection, and RNA-protein interaction analyses. Researchers can employ these cells in cholesterol efflux assays, RNA immunoprecipitation, western blotting, RT-qPCR, flow cytometry, and lipidomics to characterize molecular phenotypes. The polyclonal nature of the knockout population facilitates robust statistical analysis and allows for the assessment of heterogeneous responses. For further information or to inquire about this product, please contact Ascent Research.
