The ING4 Knockout Jurkat Polyclonal Cells are a ready-to-use CRISPR/Cas9-edited polyclonal knockout cell population, generated by disruption of the ING4 gene in the Jurkat human T lymphocyte line. This polyclonal knockout model provides a heterogeneous cell pool that avoids single-cell clonal artifacts while maintaining effective target-gene disruption, enabling robust population-level functional studies of ING4 loss in lymphoid cells.
Jurkat cells are an immortalized T lymphocyte line derived from the peripheral blood of a patient with acute T cell leukemia. They serve as a canonical model for studying T cell receptor (TCR) signaling, Fas-mediated apoptosis, and HIV infection due to their retention of key signaling components. The Jurkat background is particularly relevant for investigating the role of tumor suppressors in T-cell acute lymphoblastic leukemia (T-ALL), as it preserves sensitivity to NF-??B activation and apoptotic stimuli, allowing mechanistic dissection of ING4 in a disease-relevant context.
ING4 is a type II tumor suppressor that orchestrates cell cycle arrest, apoptosis, DNA repair, and angiogenesis inhibition. Mechanistically, ING4 associates with the HBO1 (MYST2) histone acetyltransferase complex and Tip60, promoting acetylation and activation of p53, which transcriptionally upregulates p21 and Bax. ING4 concurrently suppresses NF-??B signaling by interacting with the p65 (RELA) subunit, thereby repressing pro-survival target genes. Under hypoxia, ING4 inhibits HIF-1?? transcriptional activity, leading to reduced VEGF expression. Additionally, ING4 intersects with TGF-?? and Wnt/??-catenin pathways. Key upstream regulators include TGF-?? via Smad proteins, TNF-?? via NF-??B, and DNA damage sensing through p53. Loss of ING4 thereby disables multiple tumor-suppressive checkpoints.
In the Jurkat T cell environment, ING4 disruption is predicted to enhance proliferation and survival while diminishing apoptosis, directly mirroring its tumor-suppressive roles. This knockout model permits rigorous analysis of how ING4 loss modulates NF-??B-driven transcription and TCR-mediated apoptosis, both central to T-ALL pathogenesis. Moreover, the model enables interrogation of ING4-dependent crosstalk between p53 and HIF-1?? pathways. The polyclonal nature of the knockout pool maintains intrinsic Jurkat TCR and Fas signaling responsiveness, permitting direct phenotypic comparisons with wild-type cells in functional assays.
These cells are designed for diverse research applications, including elucidation of ING4 tumor suppressor mechanisms in T-ALL, dissection of its role in TCR-induced apoptosis and NF-??B signaling, and investigation of angiogenesis regulation. Compatible assays span Western blotting, RT-qPCR, RNA-seq, flow cytometry for apoptosis and cell cycle analysis, co-immunoprecipitation, luciferase reporter assays for p53/NF-??B activity, MTT cell viability tests, and phospho-flow analysis of signaling intermediates. They are also suited for drug sensitivity screening in leukemia models. For further information, please contact Ascent Research.
