The GOPC Knockout Jurkat Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal population of Jurkat T lymphocytes in which the GOPC (Golgi-associated PDZ and coiled-coil motif-containing) gene has been disrupted. This knockout model provides a genetically defined loss-of-function system to study GOPC-dependent processes without the confounding effects of clonal variation, as the polyclonal pool retains the diversity of a bulk-edited cell population.
The Jurkat cell line is an immortalized human T lymphocyte line originally established from the peripheral blood of a patient with acute T-cell leukemia. Widely used in immunology and cancer research, Jurkat cells serve as a robust model for T cell receptor (TCR) signaling, cytokine production, and cell proliferation studies. Their ease of culture, genetic tractability, and well-characterized signaling networks make them an ideal host for investigating the roles of adaptor proteins such as GOPC in lymphocyte biology.
GOPC encodes a PDZ domain-containing adaptor protein that localizes to the Golgi apparatus and mediates protein trafficking, receptor recycling, and intracellular signaling. GOPC interacts with key transmembrane proteins including CFTR and the frizzled receptor FZD8, linking them to the cytoskeleton and clathrin-coated vesicles via binding partners such as STX6 and BAIAP2. In the context of Wnt signaling, GOPC regulates the cell surface expression of frizzled receptors and downstream activation of the ??-catenin pathway, while also modulating GLI1 transcription factor activity in Hedgehog signaling. Upstream, GOPC function is influenced by Wnt ligands and CFTR ligands, positioning it as a critical node in integrating trafficking with signaling outputs.
Knocking out GOPC in Jurkat T cells is expected to disrupt the trafficking and surface localization of receptors such as CFTR and frizzled receptors, thereby altering downstream Wnt/??-catenin and Hedgehog pathway activity. These changes may impair T cell functions including proliferation, cytokine secretion, and immune synapse formation. Given the role of GOPC in protein sorting and its interaction with syntaxin-6 (STX6), this model provides a unique tool to dissect how Golgi-associated trafficking machinery influences T cell receptor signaling and cancer-related pathways, particularly in leukemia where Jurkat cells serve as a relevant model.
This GOPC knockout polyclonal cell population is suitable for a range of research applications including T cell signaling studies, Wnt pathway analysis, protein trafficking assays, and cancer biology research. Researchers can employ these cells in western blotting to assess protein expression changes, flow cytometry to monitor receptor surface levels, co-immunoprecipitation to probe protein?Cprotein interactions, and RT-qPCR or reporter assays to quantify transcriptional responses. Additionally, the model supports drug screening efforts aimed at identifying compounds that modulate GOPC-associated signaling networks. For further information, please contact Ascent Research.
