The BIRC2 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population of Jurkat cells with targeted disruption of the BIRC2 gene (cIAP1), providing a loss-of-function model for apoptosis and NF-??B signaling studies. This genetically heterogeneous knockout pool is derived directly from the parental Jurkat line and offers a ready-to-use reagent for functional genomics and drug screening.
Jurkat cells are an immortalized human T lymphocyte line derived from an acute T-cell leukemia patient. They grow as suspension lymphoblasts, express CD3 and the TCR, and are IL-2 independent, serving as a standard model for T-cell signaling, apoptosis, and leukemia research. Their well-defined signaling networks make them an ideal platform for CRISPR-based gene disruption.
BIRC2 encodes the E3 ubiquitin ligase cIAP1, which suppresses apoptosis by binding and ubiquitinating caspase-3, -7, and -9, thereby blocking their activation. It also promotes pro-survival NF-??B signaling by polyubiquitinating RIP1. Upon TNF-?? stimulation, BIRC2 is recruited to the TNFR1 complex via TRAF2 and modifies RIP1, leading to recruitment of the IKK complex, phosphorylation and degradation of I??B??, and subsequent NF-??B-driven transcription. Key interacting proteins include TRAF1, NIK, SMAC/DIABLO, XIAP, and cIAP2. BIRC2 is activated by upstream ligands such as TNF-??, TWEAK, and CD40L, and its loss results in enhanced caspase-8 activity and impaired NF-??B activation, shifting the balance toward apoptosis.
In Jurkat T lymphocytes, BIRC2 knockout sensitizes cells to TNF-induced apoptosis and can reveal necroptotic death, making this model valuable for studying cell death mechanisms specific to T cells. The knockout cells also allow dissection of TCR-mediated NF-??B signaling and assessment of cIAP1’s contribution to leukemic cell survival, providing a platform for therapeutic target validation.
Applications include TNF-induced apoptosis and necroptosis analysis, NF-??B pathway interrogation, IAP-targeted drug screening (e.g., Smac mimetics), and T-cell receptor signaling studies. Compatible assays comprise Western blotting for caspase activation, flow cytometry (Annexin V/PI), NF-??B luciferase reporter, co-IP of RIP1 ubiquitination, RT-qPCR, RNA-seq, and drug sensitivity assays. For additional details or technical support, please contact Ascent Research.
