The GOLGA4 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population of Jurkat T lymphocytes with disruption of the GOLGA4 gene. This heterogeneous knockout pool enables functional analysis of golgin p230, a trans-Golgi tethering factor involved in retrograde vesicle trafficking. The polyclonal format preserves the genetic diversity of the parental line, providing a physiologically relevant context for studying gene function and cellular heterogeneity in response to GOLGA4 loss-of-function. These cells are suitable for diverse biochemical, cell biological, and functional assays.
The Jurkat cell line is an immortalized human T-lymphocyte model derived from an acute lymphoblastic leukemia patient. Widely used for T-cell receptor (TCR) signaling studies, these cells express CD3, CD28, and TCR complexes, and upon activation produce cytokines. Their well-defined signaling pathways and robust growth make them an optimal host for genetic manipulation to investigate immune cell function and leukemogenesis.
GOLGA4 encodes the TGN golgin p230, a tethering factor that facilitates retrograde trafficking from endosomes to the Golgi. Its function is regulated by ARF1 GTPase, Rab6, and phosphorylation via PKA. p230 interacts with TBC1D23, GM130, and giantin to capture COPI-coated vesicles and promote SNARE-mediated fusion involving STX5 and YKT6. Disruption of GOLGA4 impairs Golgi ribbon integrity and retrograde transport, potentially disrupting protein glycosylation and secretory trafficking.
In Jurkat cells, Golgi trafficking is critical for surface receptor presentation and cytokine secretion during T-cell activation. GOLGA4 loss perturbs retrograde transport and Golgi structure, providing a model to study how such defects affect TCR signaling and downstream pathways (e.g., NF-??B, NFAT). Given the leukemic origin, this system can also reveal Golgi-related vulnerabilities in leukemia cells, complementing studies of immune cell biology.
Key applications include immunofluorescence for Golgi morphology (GM130, TGN46), Western blotting for knockout validation, flow cytometry of surface receptors (CD3, CD28), RT-qPCR for transcriptional changes, and cytokine measurement after TCR stimulation. Transcriptomic profiling by RNA-seq and chemical screening for Golgi modulators are also feasible. This polyclonal knockout model empowers research into Golgi function in T cells and its implications for immune regulation and leukemia. For further information, contact Ascent Research.
