The CCDC25 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population engineered to disrupt the CCDC25 gene. This model provides a versatile tool for probing the functional role of CCDC25 in T lymphocyte biology, with a particular emphasis on neutrophil extracellular trap (NET)-mediated signaling and its downstream consequences on cell migration and adhesion.
The Jurkat host cell line is an immortalized human T lymphocyte line established from the peripheral blood of a patient with acute T-cell leukemia (clone E6-1). Jurkat cells are widely employed in molecular and cellular immunology research because they retain key features of T-cell receptor (TCR) signaling, cytokine production, and apoptotic pathways. Their leukemic origin makes them especially relevant for studying how genes like CCDC25 may contribute to leukemogenesis and T-cell motility, bridging immunology and cancer biology.
CCDC25 functions as a receptor for extracellular DNA, specifically DNA released in neutrophil extracellular traps (NETs). Upon engagement with NET-DNA, CCDC25 activates integrin-linked kinase (ILK) and its binding partner ??-parvin, initiating a signaling cascade that converges on the small GTPases RAC1 and CDC42. This signaling module??CCDC25 ?? ILK ?? ??-parvin ?? RAC1/CDC42??orchestrates actin polymerization and cytoskeletal reorganization, thereby augmenting cell migration and invasion. The pathway underscores how NET-derived signals can be transduced into pro-metastatic cellular behaviors, with CCDC25 serving as the critical upstream sensor.
Within the Jurkat T lymphocyte milieu, disruption of CCDC25 offers a unique opportunity to dissect the intersection of NET-DNA sensing and T-cell biology. Given the involvement of T cells in immune surveillance and the leukemic background of the cell line, this knockout model can illuminate how NETs might modulate T-cell migration and potentially influence leukemic cell dissemination. Furthermore, it enables exploration of non-canonical DNA receptors in immune cells, complementing studies on TLR9 and AIM2 pathways.
This polyclonal knockout cell population is well-suited for a range of experimental approaches. NET binding assays and Transwell migration/invasion systems can directly measure the impact of CCDC25 loss on NET-driven motility. Co-immunoprecipitation and phospho-specific western blotting facilitate detailed analysis of the ILK-??-parvin signaling axis, while Rho GTPase activation pull-downs and immunofluorescence staining for NET-DNA and actin fibers visualize downstream cytoskeletal remodeling. Flow cytometry can quantify NET uptake. Additionally, these cells support high-throughput inhibitor screens and investigations into CCDC25??s role in T-cell receptor signaling. For further information or to explore this model for your research, please contact Ascent Research.
