CCDC97 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Jurkat human T lymphocyte cell line. This product enables loss-of-function studies of the CCDC97 gene, which encodes a coiled-coil domain-containing protein. The polyclonal format provides a heterogeneous population of edited cells, allowing robust assessment of gene disruption effects without clonal selection bias. Through CRISPR/Cas9-mediated gene disruption, researchers can investigate the functional consequences of CCDC97 ablation in a physiologically relevant T cell context.
Jurkat cells are an immortalized T lymphocyte line established from peripheral blood of a 14-year-old boy with acute T cell leukemia. They are widely used for studying T cell signaling pathways, activation, and leukemia biology. The Jurkat model retains key features of malignant T cells, including dysregulated proliferation and survival signaling, making it an ideal platform for investigating genes implicated in cancer. As an established model for T cell acute lymphoblastic leukemia (T-ALL), Jurkat cells provide a tractable system for genetic perturbation and phenotypic screening.
CCDC97 belongs to the coiled-coil domain-containing protein family, which typically mediates protein-protein interactions and assembly of multiprotein complexes. Although the precise role of CCDC97 remains poorly defined, it is predicted to participate in regulation of cell proliferation. Currently, no specific upstream regulators, downstream effectors, or interacting partners have been characterized. The coiled-coil architecture suggests potential involvement in scaffolding or oligomerization, but its signaling network is unknown. In the absence of defined pathway connections, knockout of CCDC97 in a cancer cell context may help uncover novel regulatory nodes or interaction partners through unbiased functional analyses.
Disrupting CCDC97 in Jurkat cells provides a valuable tool to interrogate its contribution to T cell leukemia biology. Given the protein??s potential role in proliferation control, loss-of-function studies can reveal impacts on cell cycle progression, apoptosis, and tumorigenic properties. The polyclonal knockout cell population allows the study of gene function without the artifacts of clonal selection, offering a more representative view of the knockout phenotype. This model may help identify CCDC97 dependencies that are unique to T-ALL, facilitating the discovery of therapeutic targets.
This knockout model is suited for functional characterization of CCDC97 in T cell leukemia, including genetic interaction mapping and drug sensitivity screening. Researchers can employ flow cytometry to assess apoptosis and proliferation, Western blotting to monitor signaling protein changes, MTS assays for viability, and migration assays to evaluate metastatic potential. By combining this knockout cell population with pharmacological or genetic perturbations, users can dissect the role of CCDC97 in leukemia cell fitness. For additional details or customized support, please contact Ascent Research.
