The BST2 Knockout Jurkat Polyclonal Cells provide a CRISPR/Cas9-edited polyclonal knockout cell population targeting the BST2 gene (encoding tetherin) in a human Jurkat T-lymphocyte background. This product is generated through CRISPR/Cas9-mediated gene disruption, resulting in a heterogeneous pool of cells with loss-of-function mutations, enabling robust functional studies without clonal bias. The polyclonal format preserves cellular diversity while ensuring reliable depletion of BST2 protein expression, as confirmed by standard detection methods.
The Jurkat cell line is an immortalized human T-lymphocyte line derived from an acute T-cell leukemia patient. It serves as a widely used model system for studying T-cell activation, apoptosis, and intracellular signaling cascades, including the NF-??B pathway. Jurkat cells exhibit rapid growth in suspension and are amenable to a variety of genetic manipulations, making them a versatile platform for investigating immune-related gene functions and oncogenic signaling processes.
BST2 is an interferon-inducible restriction factor that blocks the release of enveloped viruses by physically tethering budding virions to the plasma membrane. Beyond its antiviral activity, BST2 amplifies innate immune responses by activating the NF-??B transcription factor. Mechanistically, BST2 acts as a scaffold, recruiting TRAF6 and TAK1 to the IKK complex upon stimulation, which triggers phosphorylation and degradation of I??B??, releasing NF-??B for nuclear translocation. This signaling is modulated by upstream type I interferons (IFN-??/??) through the JAK-STAT cascade involving IFNAR, JAK1, TYK2, STAT1, STAT2, and IRF9, as well as by NF-??B itself, establishing a positive feedback loop that enhances proinflammatory cytokine production.
In the Jurkat cell context, BST2 knockout provides a powerful tool to dissect the dual roles of tetherin in antiviral defense and NF-??B-driven immune activation without interference from viral countermeasures like HIV-1 Vpu. The knockout model allows researchers to examine how loss of BST2 alters basal and induced NF-??B signaling, cytokine secretion profiles, and T-cell functional responses. Given that BST2 is overexpressed in hematological malignancies such as multiple myeloma, these cells are also valuable for evaluating the impact of BST2 depletion on leukemic cell proliferation and survival, aiding in target validation for cancer therapy.
These polyclonal knockout cells are suitable for a wide range of experimental applications, including viral restriction assays to quantify the release of HIV-1 and other enveloped viruses, luciferase-based NF-??B reporter assays, co-immunoprecipitation studies to assess BST2 interactions with TRAF6 and TAK1, and ELISA-based measurement of proinflammatory cytokines. They also support drug discovery efforts targeting BST2 in viral infections and multiple myeloma, with readouts such as anti-proliferation assays and qPCR for interferon-stimulated genes. For further details or to order, please contact Ascent Research.
