The ING5 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Jurkat T-lymphocyte line, designed for loss-of-function studies targeting the ING5 tumor suppressor gene. This product consists of a heterogeneous pool of cells carrying targeted disruption of ING5, enabling investigation of its role in apoptosis, cell cycle regulation, and chromatin remodeling within a physiologically relevant T-cell leukemia background.
The Jurkat cell line is an immortalized human T-lymphocyte line originally established from an acute T-cell leukemia patient. These suspension cells are widely employed in immunological and cancer research to dissect T-cell receptor signaling, immune response mechanisms, and leukemogenesis. Their well-characterized signaling pathways and genetic tractability render them an ideal host for CRISPR-based gene disruption, particularly for exploring tumor suppressor functions such as those mediated by ING5.
ING5 functions as a tumor suppressor by serving as a subunit of the HBO1 histone acetyltransferase (HAT) complex, which acetylates histones H3 and H4 to promote chromatin relaxation and transcriptional activation. It cooperates directly with p53 to enhance the expression of pro-apoptotic genes such as BAX and PUMA, as well as cell cycle regulators including p21 and cyclin B1. Upstream signals from p53, MYC, and E2F1 can regulate ING5 expression, while ING5 interacts with HBO1, ING4, BRPF1, MORF4, and JADE within the HAT complex. Downstream, ING5-mediated acetylation events facilitate p53-dependent apoptosis and cell cycle arrest, ultimately leading to caspase-3 activation. This positions ING5 at a critical intersection of the DNA damage response and epigenetic regulation.
In the Jurkat T-cell leukemia context, disruption of ING5 provides a powerful model to dissect its tumor-suppressive functions under conditions of aberrant T-cell signaling and leukemogenesis. Since Jurkat cells harbor mutations in key pathways, including p53, the ING5 knockout system enables investigation of p53-independent and -dependent mechanisms of apoptosis and cell cycle regulation. The polyclonal population mirrors a range of disruption efficiencies and clonal variation, allowing researchers to observe phenotypic heterogeneity akin to that seen in tumor evolution. This model is especially suited for studying how loss of ING5 impacts histone acetylation landscapes, DNA damage responses, and sensitivity to chemotherapeutic agents.
The ING5 Knockout Jurkat Polyclonal Cells are suitable for a broad range of research applications, including investigation of tumor suppressor mechanisms, apoptosis and cell cycle analyses, and drug sensitivity screening in T-cell leukemia. Typical assays include Western blotting and RT-qPCR for expression analysis, flow cytometry with annexin V/PI staining for apoptosis detection, cell cycle progression studies, and colony formation assays to assess proliferation. Co-immunoprecipitation and ChIP-qPCR can be employed to characterize interactions with HBO1 or p53 and histone modification changes, while RNA-seq provides genome-wide transcriptional profiling. Caspase activity assays further characterize apoptotic pathways. For further information, please contact Ascent Research.
