The CASP7 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Jurkat T lymphocyte cell line, in which the CASP7 gene has been disrupted. This polyclonal population provides a reliable loss-of-function model for investigating caspase-7-dependent biological processes without the need for single-cell cloning. The polyclonal format maintains genetic diversity while offering consistent target-gene disruption, making it suitable for a range of experimental applications in apoptosis and immune cell signaling.
Jurkat cells, originally isolated from the peripheral blood of a 14-year-old male with acute T cell leukemia, serve as a well-established model for studying T cell receptor signaling, apoptosis, and leukemia biology. Their ease of culture, robust signaling responses, and well-characterized genetic background have made Jurkat cells a cornerstone in immunology and cancer research, particularly for dissecting the molecular mechanisms governing T cell activation and programmed cell death.
CASP7 encodes caspase-7, an executioner caspase that plays a central role in apoptosis. Upon activation by initiator caspases such as caspase-8 and caspase-9 via the extrinsic and intrinsic apoptotic pathways, respectively, caspase-7 cleaves key cellular substrates including PARP, ??-fodrin, gelsolin, and ICAD, leading to DNA fragmentation and cell dismantling. Caspase-7 can also be activated downstream of caspase-3 and granzyme B, and its activity is tightly regulated by inhibitor of apoptosis proteins (IAPs) such as XIAP, cIAP1/2, and Survivin. The caspase-7 signaling network integrates signals from the DISC complex, apoptosome, and p53 pathways, placing it at a critical node in the caspase cascade.
Disruption of CASP7 in Jurkat cells impairs the execution phase of apoptosis, conferring resistance to both death-receptor-mediated and mitochondria-dependent apoptotic stimuli. This knockout model is particularly valuable for dissecting the specific functions of caspase-7 in T lymphocyte apoptosis and for interrogating the interplay between caspase-7 and other executioner caspases. Moreover, it enables the study of caspase-7’s non-apoptotic roles in differentiation and inflammation, providing insights into pathways that may be dysregulated in leukemia and other cancers.
These CASP7 knockout polyclonal cells are ideally suited for a wide range of research applications, including apoptosis research, cancer drug resistance studies, T cell signaling analysis, and leukemia biology. They can be used in caspase activity assays, Western blotting for caspase-7 cleavage, flow cytometry-based apoptosis assays (e.g., Annexin V/PI staining), and drug sensitivity screens to identify pro-apoptotic compounds. Additionally, RNA-seq and co-immunoprecipitation experiments can help elucidate the broader impact of CASP7 loss on gene expression and protein interaction networks. For further details, please contact Ascent Research.
