The AKNA Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from Jurkat human T lymphocytes, offering targeted disruption of the AKNA gene. This heterogeneous pool contains cells with diverse loss-of-function modifications, enabling study of AKNA-dependent functions without clonal selection artifacts. The polyclonal format provides a robust model for investigating gene function in T cell biology and inflammatory signaling.
The Jurkat cell line, an immortalized T lymphocyte model derived from acute T cell leukemia, is widely used to study adaptive immune responses, including TCR signaling and cytokine production. Jurkat cells exhibit NF-??B pathway activation upon stimulation, making them a standard platform for dissecting transcriptional regulation in T cell activation and inflammation. Their leukemic origin also supports research into aberrant signaling in T cell malignancies.
AKNA is an AT-hook transcription factor that orchestrates immune gene expression by interacting with NF-??B p65, p300/CBP, and HDACs. It is activated by TNF-??, IL-1??, and TCR signaling, and promotes transcription of downstream targets such as IL-6, IL-8, CXCL1, and CCL20. Within the NF-??B cascade, AKNA integrates signals from the IKK complex and I??B?? to modulate p65 activity at cytokine promoters. Disruption of AKNA thereby impairs NF-??B-mediated inflammatory signaling and cytokine production.
In Jurkat T cells, AKNA knockout compromises the expression of key inflammatory mediators, providing a functional readout for T cell activation deficits. This model is particularly valuable for dissecting how TCR and cytokine receptor inputs converge on AKNA to control transcriptional programs that govern adaptive immunity. The polyclonal nature offers broad phenotype representation, facilitating screening assays and mechanistic studies of NF-??B-driven inflammation.
Applications include inflammation research, T cell immunology, and drug screening for anti-inflammatory compounds. Standard assays such as RT-qPCR for cytokine mRNA, ELISA for secreted IL-6 and IL-8, flow cytometry for activation markers, and NF-??B reporter assays are readily applied. The model also supports cancer biology studies exploring T cell signaling dysregulation. For further details, please contact Ascent Research.
