The CCDC85C Knockout Jurkat Polyclonal Cells product comprises a CRISPR/Cas9-edited polyclonal population of Jurkat T lymphoblastoid cells in which the CCDC85C gene has been disrupted to create a loss-of-function model. This polyclonal knockout cell pool is generated via CRISPR/Cas9-mediated gene disruption, providing a genetically heterogeneous population suitable for studying the effects of CCDC85C deficiency without the selection bottlenecks inherent to clonal isolation. The engineered cells retain their immortalized T lymphocyte characteristics and serve as a versatile tool for functional genomics and phenotypic screening applications in a human T cell context.
The Jurkat cell line is an immortalized human T lymphocyte model derived from an acute T cell leukemia patient, widely used for T cell receptor signaling, apoptosis, and leukemia research. Jurkat cells grow in suspension, bear constitutive TCR pathway activation, and harbor mutations in key tumor suppressors, rendering them a robust system for cancer studies. This well-characterized background provides a relevant context for examining centrosomal protein functions in lymphocyte biology and malignant transformation.
CCDC85C is a coiled-coil domain-containing centrosomal protein that localizes to centrosomes and procentrioles, playing a critical role in centriole duplication. It interacts directly with CEP170 and operates within the centriole biogenesis network that includes PLK4, CEP152, STIL, SASS6, and CPAP. Upstream regulators PLK4 and CDK2 coordinate CCDC85C activity with cell cycle progression, ensuring fidelity of procentriole assembly. Through these interactions, CCDC85C influences centrosome maturation, mitotic spindle formation, and ciliogenesis. Disruption of this gene may cause centriole duplication errors, centrosome amplification, and defective ciliary function.
In Jurkat T leukemia cells, CCDC85C-dependent centrosome regulation likely contributes to the uncontrolled proliferation associated with acute T cell leukemia. Centrosome anomalies can promote chromosomal instability and tumor growth, making this model valuable for studying how centrosomal protein disruption affects leukemic progression. Moreover, the link between ciliogenesis and cell cycle arrest raises the possibility that impaired cilia formation in T cells alters signaling pathways relevant to leukemia maintenance. The polyclonal knockout population captures variant alleles, enabling robust phenotypic analysis without clonal bias.
These CCDC85C knockout cells support diverse experimental workflows, including immunofluorescence microscopy for centrosome visualization (e.g., ??-tubulin, centrin), centriole duplication assays, and cell cycle flow cytometry. Co-immunoprecipitation studies using CEP170 enable investigation of altered centrosomal interactions, while proliferation and cilia formation assays assess functional consequences. Western blotting confirms target gene disruption. The product is also suited for exploring non-canonical functions of CCDC85C in T cell signaling. For further details, contact Ascent Research.
