The BCL10 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population with targeted disruption of the BCL10 gene in human Jurkat T lymphoblasts. This polyclonal model provides a heterogeneous gene-disrupted pool for functional studies of BCL10-dependent signaling pathways. The genetic disruption is achieved through CRISPR/Cas9-mediated targeting, resulting in abrogation of BCL10 protein expression across the cell pool. It serves as a versatile tool for investigating NF-??B signaling in T-cell biology.
Jurkat cells are an immortalized human T lymphoblast line derived from acute T-cell leukemia, widely employed as a model for T-lymphocyte activation and signal transduction. They retain robust TCR complex expression and downstream signaling machinery, responding potently to anti-CD3/CD28 stimulation or pharmacological PKC activators such as PMA/ionomycin. This well-characterized background enables reproducible interrogation of TCR-mediated NF-??B activation.
BCL10 functions as a CARD-containing adaptor protein essential for NF-??B activation downstream of antigen receptors. Upon TCR engagement, Lck and ZAP-70 trigger PLC??1, leading to PKC??-mediated phosphorylation of CARMA1. BCL10 then oligomerizes and recruits MALT1 and TRAF6, forming the CBM signalosome. TRAF6 promotes TAK1 activation, which phosphorylates the IKK complex. Active IKK mediates I??B?? degradation, releasing NF-??B (p50/p65) for nuclear translocation and transcription of genes such as IL-2 and TNF-??. BCL10 thus operates downstream of CARMA1 and upstream of the IKK complex.
In Jurkat cells, BCL10 knockout disrupts the TCR-NF-??B axis, offering a physiologically relevant model to examine signal requirements for T-cell activation. Loss of BCL10 impairs IKK activity and NF-??B-driven cytokine production, mirroring signaling defects observed in certain immunodeficiencies. The leukemic origin of Jurkat cells further enables investigation of BCL10 mutations associated with MALT lymphoma, highlighting its dual roles in immune homeostasis and neoplasia.
Key applications include NF-??B pathway inhibitor screening, mechanistic studies of TCR/CD28 costimulatory signaling, and validation of the BCL10-MALT1 interaction as a therapeutic target. Representative assays encompass NF-??B luciferase reporter measurements, western blot analysis of I??B?? phosphorylation, flow cytometric quantification of CD69, IL-2 ELISA, and co-immunoprecipitation of CBM complex components. This polyclonal knockout population is suitable for research in immunology, cancer biology, and drug discovery. For further information, please contact Ascent Research.
