The ANAPC16 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population for loss-of-function studies of ANAPC16 in human T lymphocytes. This polyclonal population carries targeted gene disruptions generated by Cas9-mediated cleavage, providing a heterogeneous model that avoids clonal selection artifacts. The cells are suitable for investigating gene function in cell cycle progression and ubiquitin-dependent proteolysis.
Jurkat cells are an immortalized T-cell line derived from the peripheral blood of a male patient with acute T-cell leukemia. Widely used to study T-cell receptor signaling, apoptosis, and leukemogenesis, Jurkat cells grow in suspension and are compatible with flow cytometry and high-throughput assays. Their transformed phenotype makes them an ideal host for exploring oncogenic mechanisms in T-cell malignancies.
ANAPC16 encodes an essential subunit of the anaphase-promoting complex/cyclosome (APC/C), an E3 ubiquitin ligase that controls the metaphase-to-anaphase transition by targeting proteins for degradation. The APC/C is activated by co-activators CDC20 and CDH1 and regulated by kinases CDK1 and PLK1. ANAPC16 interacts with core APC/C subunits ANAPC1 and ANAPC2 to maintain complex function. Key substrates include cyclin B1 and securin, whose degradation triggers mitotic exit, and Aurora A and NEK2A, which are additional APC/C targets. Thus, ANAPC16 is critical for accurate chromosome segregation and mitotic progression.
Knockout of ANAPC16 in Jurkat cells disrupts APC/C activity, leading to accumulation of cyclin B1 and securin, mitotic arrest, and genomic instability. These phenotypes mirror defects observed in T-cell acute lymphoblastic leukemia, where deregulated cell cycle control contributes to pathogenesis. The polyclonal knockout population recapitulates genetic heterogeneity, enabling researchers to study ANAPC16 loss in a context relevant to tumor biology without the limitations of single-cell clones. This model thus provides a powerful system to interrogate the interplay between APC/C dysfunction and T-cell transformation.
This knockout model supports a range of experimental approaches, including flow cytometric cell cycle analysis, Western blotting for cyclin B1 and securin, proliferation and apoptosis assays, and in vitro ubiquitination assays. It is well-suited for functional genomics screens, drug target validation, and investigation of synthetic lethal interactions involving the APC/C pathway. For further details and technical assistance, please contact Ascent Research.
