The DOCK10 Knockout HeLa Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population designed to introduce loss-of-function mutations in the human DOCK10 gene within the HeLa cell background. This polyclonal model provides a heterogeneous pool of edited cells, enabling researchers to study DOCK10-dependent cellular processes without the clonal selection biases associated with monoclonal cell lines. The product is optimized for applications in cell migration, cytoskeletal dynamics, and Rho GTPase signaling research.
HeLa cells, derived from a human cervical adenocarcinoma, are an immortalized epithelial cell line widely employed as a model system for cancer biology, virology, and signal transduction studies. Their robust growth, genetic tractability, and well-characterized signaling networks make them particularly suitable for CRISPR-based loss-of-function analyses. The epithelial morphology and intrinsic migratory capacity of HeLa cells provide a physiologically relevant platform for dissecting the molecular mechanisms governing cell polarity, adhesion, and motility.
DOCK10 encodes a guanine nucleotide exchange factor (GEF) that specifically activates the Rho GTPases Cdc42 and Rac1 through its DHR2 catalytic domain. Upon interaction with the adaptor protein ELMO1, DOCK10 catalyzes the exchange of GDP for GTP on Cdc42 and Rac1, which in turn stimulates downstream effectors including PAK kinases, WASP/WAVE complexes, and the Arp2/3 complex to promote actin polymerization and lamellipodia formation. Upstream regulators such as receptor tyrosine kinases, G protein-coupled receptors, and phosphatidylinositol 3-kinase modulate DOCK10 activity, linking extracellular cues to cytoskeletal reorganization. The DOCK10 signaling axis also intersects with LIMK and cofilin pathways, further regulating actin dynamics and cell migration.
In HeLa cells, loss of DOCK10 function is anticipated to impair Cdc42 and Rac1 activation, leading to defects in actin remodeling, lamellipodia formation, and directional cell migration. Given the established role of DOCK10 in immune cell function and cancer progression, this knockout model provides a valuable tool for investigating the contribution of DOCK10 to the invasive behavior of cervical adenocarcinoma cells. Additionally, the polyclonal nature allows for the study of heterogeneous cellular responses and reduces artifacts that may arise from single-cell-derived clones.
Researchers can employ these DOCK10 polyclonal knockout HeLa cells in a variety of assays to characterize migratory and cytoskeletal phenotypes, including Transwell migration, wound healing, and phalloidin staining for F-actin. The model is also suitable for biochemical analyses such as Cdc42/Rac1 GTPase activation pull-downs and western blotting for downstream effectors like PAK1 and LIMK. Time-lapse live-cell imaging and immunofluorescence for lamellipodia markers further enable real-time visualization of DOCK10-dependent processes. This reagent supports investigations into cancer metastasis, immune dysregulation, and Rho GTPase signaling networks. For additional information or technical support, please contact Ascent Research.
