CCDC14 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Jurkat human T-lymphocyte leukemia cell line. This product contains a heterogeneous pool of Jurkat cells carrying targeted disruptions in the CCDC14 gene, generated by CRISPR/Cas9-mediated gene editing. The resulting polyclonal knockout model enables loss-of-function studies of CCDC14 within a T-cell context, without requiring single-cell cloning. As a polyclonal pool, it retains diverse editing events across the cell population, providing a representative CCDC14-deficient background for functional assays.
The parental Jurkat cell line is a well-characterized suspension cell model derived from the peripheral blood of an acute T-cell leukemia patient. Jurkat cells express CD4 and are widely used to investigate T-cell receptor signaling, apoptosis, and leukemogenesis. Their robust proliferation and genetic tractability make them an ideal platform for generating gene knockouts to explore molecular mechanisms underlying T-cell malignancies. Consequently, CCDC14 disruption in Jurkat cells provides a disease-relevant system for studying centrosome-related defects in leukemia.
CCDC14 encodes a centrosomal protein essential for centriole duplication and mitotic spindle assembly. It interacts directly with CEP63 and CEP152 to facilitate the recruitment of PLK4 to the centrosome, a critical step in centriole biogenesis. Upstream, CCDC14 is regulated by PLK4 and CDK2, while downstream signaling involves key centrosomal components including SAS6, STIL, CPAP, and CEP135. Through these interactions, CCDC14 coordinates centriole formation and ensures proper chromosome segregation during mitosis. Disruption of this network leads to centrosomal abnormalities, genomic instability, and cell cycle defects, which are particularly relevant in rapidly dividing cancer cells.
In the Jurkat leukemia background, CCDC14 knockout provides a powerful model to dissect the role of centrosome duplication in T-cell proliferation and survival. Because Jurkat cells are highly proliferative, they are susceptible to mitotic errors resulting from impaired centriole assembly. This polyclonal knockout population allows researchers to examine how loss of CCDC14 affects centrosome number, spindle morphology, and cell cycle progression in a leukemia-relevant context. Moreover, the model connects centrosomal dysregulation to pathologies such as microcephaly and cancer, enabling translational studies on centrosome-targeted therapeutic strategies.
This knockout cell product is well-suited for a range of experimental approaches, including Western blotting and RT-qPCR to confirm CCDC14 absence, immunofluorescence microscopy for centrosome and spindle visualization, flow cytometry to monitor cell cycle distribution and apoptosis, and proliferation assays to assess growth defects. Typical research applications include investigating the molecular details of centriole duplication, evaluating mitotic checkpoint fidelity in leukemia, and screening centrosome-targeted compounds for anticancer activity. For further information, please contact Ascent Research.
