CCDC167 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Jurkat T lymphoblastoid cell line, featuring targeted disruption of the CCDC167 gene. This population-based knockout model avoids clonal selection, offering a physiologically relevant system for investigating ESCRT-dependent pathways.
The parental Jurkat line is an immortalized human T lymphocyte established from a patient with acute lymphoblastic leukemia. It serves as a widely adopted model for T cell signaling, activation, and apoptosis, and is permissive to HIV-1 infection, enabling robust studies of viral replication and host-virus interactions.
CCDC167 is a core component of the ESCRT-I complex, which mediates membrane scission events including multivesicular body formation, viral budding, and cytokinetic abscission. Within ESCRT-I, CCDC167 interacts with Tsg101, VPS28, and VPS37, and facilitates recruitment of ALIX (PDCD6IP) and ESCRT-III subunits such as CHMP4B and VPS4A. HIV-1 Gag exploits CCDC167 to promote viral particle release from the plasma membrane, while during cell division, CCDC167 localizes to the midbody to enable membrane abscission. Upstream regulatory mechanisms remain unclear, though cell cycle kinases may modulate its function.
In Jurkat cells, CCDC167 knockout disrupts the assembly and function of the ESCRT-I complex, leading to impaired HIV-1 budding and reduced viral release. This enables detailed dissection of ESCRT-dependent viral egress steps. Additionally, defective cytokinetic abscission results in multinucleated cells and increased apoptosis, providing insights into the role of ESCRT proteins in maintaining genomic stability and T cell proliferation. Such phenotypes link CCDC167 loss to potential oncogenic processes, making this model valuable for both virology and cancer research.
These polyclonal knockout cells are ideally suited for a range of functional assays. HIV-1 release assays can quantify budding efficiency, while flow cytometry enables cell cycle profiling and detection of multinucleation. Western blotting can assess expression levels of ESCRT components such as Tsg101, ALIX, and CHMP4B, and immunofluorescence can visualize midbody defects and abscission failure. Co-immunoprecipitation studies are facilitated to map ESCRT interactions. Furthermore, the cells serve as a platform for antiviral drug screening targeting HIV-1 assembly. For further technical details or to discuss your experimental needs, please contact Ascent Research.
