The APOB Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population of Jurkat human T lymphoblasts with targeted disruption of the APOB gene. This heterogeneous pool of edited cells enables study of APOB loss-of-function phenotypes while preserving population diversity inherent to polyclonal editing.
The Jurkat cell line, an immortalized T lymphocyte line derived from a 14-year-old male with acute T cell leukemia, exhibits suspension lymphoblast morphology and is a standard model for T cell signaling, activation, and leukemogenesis. Its well-characterized signaling networks and rapid growth facilitate CRISPR-based gene editing for investigating genes involved in lipid metabolism within a lymphoid context.
APOB encodes apolipoprotein B, the core structural protein of atherogenic VLDL and LDL, required for their assembly and secretion via interaction with microsomal triglyceride transfer protein (MTP). APOB mediates LDL receptor (LDLR)-dependent endocytosis, modulating cholesterol delivery to peripheral tissues. APOB expression is regulated by HNF4A, FOXO1, miR-122, insulin, and statins, and influences downstream effectors such as LDLR, lipoprotein lipase, and CETP. APOB also interacts with HSPG and is indirectly affected by PCSK9-mediated LDLR degradation. Thus, APOB disruption abolishes VLDL/LDL structural integrity, impairing lipoprotein secretion and cellular cholesterol homeostasis.
In Jurkat T cells, APOB knockout provides insights into the interplay between lipid homeostasis and immune function. Although T cells are not primary lipoprotein secretors, cholesterol-rich lipid rafts are crucial for T cell receptor (TCR) signaling and activation. APOB loss may alter membrane cholesterol content and raft dynamics, potentially modifying TCR-mediated signaling cascades and leukemic cell survival, making this model valuable for exploring lipid-dependent vulnerabilities in T-cell leukemia.
These polyclonal knockout cells can be utilized in LDL uptake assays, cholesterol efflux measurements, Western blotting for APOB and LDLR, RT-qPCR for APOB mRNA, Oil Red O staining, and flow cytometry for LDLR surface expression. They enable proteomic studies such as co-immunoprecipitation of APOB with MTP, as well as metabolic flux analyses and viability assessments under lipid deprivation. The model supports drug screening for APOB regulators and functional studies of lipoprotein biology in lymphocytes. For additional information, contact Ascent Research.
