The ACTR5 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population designed for loss-of-function studies of the ACTR5 gene. Derived from the Jurkat T lymphocyte cell line, this polyclonal model carries targeted disruptions of ACTR5, enabling researchers to interrogate the gene’s function in human immune cells. As a pooled population, it reflects heterogeneous editing events and is suited for bulk cellular analyses without clonal selection.
Jurkat cells are an immortalized human T lymphocyte line originally derived from the peripheral blood of a leukemia patient. Widely employed in T-cell signaling, adaptive immunity, and cancer biology research, they provide a physiologically relevant background for studying chromatin remodeling and gene regulation in the context of immune function. Their robust proliferative capacity and well-characterized signal transduction pathways??including TCR/CD3-mediated activation??make them a versatile host for genomic perturbation.
ACTR5 encodes a core subunit of the INO80 chromatin remodeling complex, an ATP-dependent molecular machine that mobilizes nucleosomes to regulate DNA accessibility. INO80 activity is triggered by DNA damage signals through upstream kinases such as ATM and ATR, and is also modulated by transcription factors including YY1 and MYC. ACTR5 interacts directly with INO80, RUVBL1, RUVBL2, actin, ARP4, ARP8, and YY1 within the complex. Once activated, the complex catalyzes nucleosome eviction at promoters and H2A.Z histone variant exchange, facilitating transcriptional activation of damage-responsive genes. Thus, ACTR5 sits at the nexus of chromatin structure, DNA double-strand break repair, and transcriptional reprogramming, and its disruption compromises genome stability.
In Jurkat cells, knockout of ACTR5 impairs assembly of the INO80 complex, leading to defective DNA damage response and altered gene expression profiles. Given the central role of T lymphocytes in adaptive immunity and their susceptibility to genomic lesions, this polyclonal model is particularly relevant for dissecting how chromatin dynamics influence T-cell activation, proliferation, and malignant transformation. Key downstream consequences include failure to resolve ??-H2AX foci, reduced chromatin remodeling ATPase activity, and aberrant transcriptional outputs, as can be assessed by immunofluorescence, comet assays, and western blotting for INO80 subunits.
The ACTR5 Knockout Jurkat Polyclonal Cells support a wide range of experimental applications, including mechanistic studies of chromatin remodeling, DNA damage signaling, and cancer epigenetics. Researchers can employ RNA sequencing to profile transcription changes, flow cytometry to monitor cell cycle perturbations, and chromatin remodeling assays to measure ATPase activity. This model is also suited for pharmacological screening to identify compounds that target INO80-dependent pathways. Researchers interested in utilizing this model are encouraged to contact Ascent Research for detailed protocols and technical support.
