The GOLGA3 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population with disruption of the GOLGA3 gene, which encodes a golgin protein essential for Golgi ribbon maintenance. This heterogeneous pool of Jurkat T lymphocytes captures a spectrum of gene-editing events, providing a robust loss-of-function model free of clonal selection bias.
Jurkat cells are an immortalized human T lymphocyte line derived from the peripheral blood of a patient with acute T cell leukemia. They serve as a well-established model system for T cell receptor (TCR) signaling, cytokine production, calcium flux, and apoptosis, and are widely utilized in both immunological and cancer research.
GOLGA3 encodes a cis-Golgi golgin that tethers vesicles and organizes cisternal stacking through interactions with GM130 (GOLGA2), p115, syntaxin 5, the COPI coat complex, and the small GTPases ARF1 and RAB1. Its function is regulated by mitotic kinases CDK1 and PLK1, which phosphorylate GOLGA3 to control Golgi dynamics, while RAB GTPases mediate membrane recruitment. Knockout of GOLGA3 results in Golgi fragmentation, defective anterograde and retrograde vesicular trafficking, and altered cell surface glycosylation, thereby impairing receptor expression and downstream signaling.
In Jurkat T lymphocytes, the Golgi ribbon is critical for proper glycosylation and surface presentation of TCR components and co-receptors, as well as for polarized cytokine secretion. GOLGA3 disruption compromises Golgi structural integrity, leading to attenuated TCR-mediated calcium responses and immune activation. This model is thus invaluable for investigating how Golgi dysfunction contributes to T-cell leukemia pathogenesis and immune dysregulation.
This polyclonal knockout cell population is suitable for immunofluorescence imaging of Golgi markers (e.g., GM130, TGN46), flow cytometry with lectins to quantify glycosylation changes, western blotting for Golgi matrix proteins, and RT-qPCR for trafficking-related genes. Functional assays such as TCR-stimulated calcium mobilization, apoptosis detection, and cell migration assays enable dissection of Golgi-dependent T-cell behavior. The model also supports drug screening for Golgi-disrupting agents in cancer. For further technical inquiries, contact Ascent Research.
