The INO80C Knockout Jurkat Polyclonal Cells provide a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Jurkat human T-lymphocyte line, with targeted disruption of the INO80C gene. This polyclonal format offers a bulk loss-of-function model suitable for studying chromatin remodeling without clonal selection artifacts, applicable to a broad range of biochemical and functional assays.
Jurkat cells are a widely used human T-cell leukemia model, originating from acute lymphoblastic leukemia. They recapitulate key aspects of T-cell signaling and immune response, and their robust growth and genetic tractability make them an optimal host for CRISPR-based gene knockout studies in a malignant lymphoid context.
INO80C is an essential subunit of the INO80 ATP-dependent chromatin remodeling complex, which utilizes ATP hydrolysis to reposition nucleosomes and modulate DNA accessibility. Within the complex, INO80C interacts with INO80, RUVBL1/2, ARP5/8, ACTL6A, and the transcription factor YY1 to regulate transcription, DNA repair, and replication fork dynamics. The complex is activated by ATM and ATR kinases in response to DNA double-strand breaks and replication stress, promoting downstream events such as RAD51 recruitment to damage sites, H2AX phosphorylation, and altered expression of cell cycle genes.
In Jurkat T-cells, INO80C knockout disrupts INO80 complex function, impairing chromatin remodeling necessary for proper DNA damage responses and transcriptional regulation. This deficiency likely leads to increased genomic instability and altered T-cell signaling, reflecting the oncogenic processes in leukemia and lymphoma. The model is valuable for dissecting how chromatin dynamics contribute to malignant transformation and drug resistance.
This knockout cell population enables diverse research applications including chromatin immunoprecipitation (ChIP)-qPCR to assess histone modifications, immunofluorescence for DNA damage foci, comet assays for DNA break detection, and flow cytometry for cell cycle profiling. Transcriptomic analysis by RNA-seq and chromatin accessibility mapping by ATAC-seq further elucidate genome-wide regulatory changes. The cells are also suited for clonogenic survival assays and screening of chromatin remodeling inhibitors. For further information, please contact Ascent Research.
