The BCL3 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population targeting the BCL3 gene in the Jurkat human CD4+ T lymphocyte line. This product comprises a heterogeneous pool of cells carrying diverse gene disruptions at the BCL3 locus, offering a robust functional knockout model that circumvents clonal selection artifacts. The polyclonal format maintains genetic diversity while delivering consistent loss-of-function phenotypes in population-level assays, making it suitable for high-throughput screening and pooled functional genomics approaches.
The Jurkat cell line is an immortalized suspension line isolated from the peripheral blood of an acute T cell leukemia patient. It is extensively utilized as a model system for T cell receptor (TCR) signaling, T cell activation, HIV infection, and leukemia biology. Jurkat cells recapitulate many aspects of CD4+ T lymphocyte physiology, including inducible NF-??B activation and cytokine secretion, and their well-characterized signal transduction network provides an ideal platform for dissecting the molecular mechanisms of immune regulation and oncogenesis.
BCL3 encodes a transcriptional coactivator that specifically associates with NF-??B p50 and p52 homodimers to promote expression of genes controlling proliferation, survival, and immune responses. Its activity is triggered by extracellular stimuli such as TNF-??, IL-1??, and LPS, which signal through the canonical NF-??B pathway involving receptors like TLR4, adaptors MYD88 and IRAK1, and kinases IKBKB and CHUK. Upon activation, BCL3 interacts with NFKB1 (p50) and NFKB2 (p52), and with co-regulators including COPS5 (Jab1), HDAC1, and PIR. Post-translational modifications such as phosphorylation and ubiquitination fine-tune BCL3 activity, enabling context-dependent regulation of target genes such as CCND1, MYC, BCL2, IL6, and SPP1.
In Jurkat cells, disruption of BCL3 impairs NF-??B-driven transcriptional programs that are essential for leukemic cell proliferation and survival. Jurkat cells exhibit high basal NF-??B activity characteristic of many T cell malignancies; thus, BCL3 knockout allows researchers to dissect the specific contribution of p50/p52 homodimer-mediated transcription distinct from that of other NF-??B dimer configurations. This model is particularly valuable for studying T cell activation, cytokine production, anti-apoptotic mechanisms, and drug resistance, and it serves as a relevant system for exploring BCL3 as a therapeutic target in leukemia and lymphoma.
Research applications include detailed investigation of the NF-??B signaling network, T cell biology, CRISPR-based functional genomics, and inflammatory signal transduction. Representative experimental techniques enabled by this knockout model are Western blotting, RT-qPCR, NF-??B reporter assays, flow cytometry, co-immunoprecipitation, cytokine ELISA, proliferation assays, and RNA-seq. For further technical details or to discuss custom gene editing services, please contact Ascent Research.
