The CCDC127 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population designed to disrupt the human CCDC127 gene within the Jurkat T lymphocyte line. This product provides a heterogeneous pool of knockout cells, enabling robust loss-of-function studies without clonal selection. By targeting CCDC127, these cells serve as a versatile model for investigating centriole biogenesis, ciliogenesis, and related cell cycle processes, while preserving the native signaling context of an immortalized T cell background.
Jurkat cells are an extensively characterized immortalized human T lymphocyte line derived from an acute T cell leukemia patient. They maintain key attributes of T cell biology, including active T cell receptor (TCR) signaling and intact apoptotic machinery, making them a gold-standard model for studying immune response mechanisms, signal transduction, and programmed cell death. Their robust growth and genetic manipulability facilitate high-throughput genetic screens and detailed mechanistic investigations in a well-defined cellular environment.
CCDC127 encodes a coiled-coil domain-containing protein that localizes to centriolar satellites and plays a critical role in centriole duplication and primary cilium assembly. It functions as a scaffolding component, interacting with centriolar satellite proteins such as CEP290, PCM1, and PLK1 to regulate the recruitment of ciliogenesis factors to the centrosome. Its activity is modulated by cell cycle-dependent kinases, including CDK1 and PLK1, and its loss disrupts the organization of centrosomal proteins and ciliary membrane components, thereby impairing ciliogenesis and potentially affecting cell cycle progression at the G2/M transition.
In Jurkat T cells, CCDC127 knockout offers a unique window into the intersection of centriole biology and immune cell function. Although T lymphocytes are non-ciliated under normal conditions, the centrosome remains pivotal for cell division and intracellular signaling, including pathways downstream of the TCR. Disrupting CCDC127 can therefore reveal how centriolar satellite dysfunction influences T cell proliferation, polarity, and signaling dynamics, with broader implications for understanding ciliopathy-associated immune dysregulation.
This polyclonal knockout model supports diverse applications such as examining centriole biogenesis and ciliogenesis in a T cell context, investigating CCDC127-dependent cell cycle regulation, and modeling molecular aspects of ciliopathies like Meckel and Joubert syndromes. Researchers can employ established assays including Western blotting and RT-qPCR for target expression analysis, immunofluorescence microscopy to visualize centriolar markers (??-tubulin, CEP290) and ciliary structures, and flow cytometry for cell cycle profiling. Ciliogenesis assays under serum-starvation conditions further enable functional readouts of primary cilium assembly. For customized bulk orders or technical inquiries, please contact Ascent Research.
