DOCK9 Knockout HeLa Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population of HeLa cells carrying targeted disruption of the DOCK9 gene locus, providing a heterogeneous loss-of-function model for investigating DOCK9-dependent cellular processes. This polyclonal knockout product avoids clonal-selection artifacts and enables study of gene function within a mixed genetic background that better reflects natural biological variability.
The host HeLa cell line is an immortalized epithelial line derived from a human cervical adenocarcinoma, positive for HPV18, with E6-mediated p53 degradation. HeLa cells exhibit an adherent morphology, aneuploid karyotype, and are extensively utilized as a robust platform for cancer biology, virology, and drug discovery, particularly in assays of cell migration, invasion, and cytoskeletal dynamics.
DOCK9 encodes a guanine nucleotide exchange factor (GEF) that specifically activates the Rho GTPases Cdc42 and Rac1 by promoting GDP/GTP exchange. Activated Cdc42 and Rac1 trigger downstream effectors including PAK kinases (PAK1?C3), which regulate actin polymerization through WASP/WAVE-family proteins and the Arp2/3 complex, leading to F-actin reorganization, lamellipodia and filopodia formation, and focal adhesion dynamics. Upstream inputs such as receptor tyrosine kinases (e.g., EGFR, PDGFR), the small GTPase RhoG, and PIP3 modulate DOCK9 activity, while adaptor proteins ELMO1 and NCK participate in DOCK9-mediated signaling complexes.
Within HeLa cells, disruption of DOCK9 is expected to impair Cdc42/Rac1-driven actin remodeling and cell motility. This model is thus particularly relevant for dissecting the contribution of DOCK9-dependent GTPase signaling to the invasive phenotype of cervical adenocarcinoma cells and for assessing pharmacological inhibition of GEF activity.
Key applications include wound healing and transwell migration/invasion assays to quantify cell motility, phalloidin staining to examine F-actin architecture, Western blotting for phospho-PAK as a pathway activity readout, and GST-PAK-CRIB effector pull-downs to directly measure Cdc42/Rac1 activation. These polyclonal knockout cells are also suitable for GEF inhibitor screening and for modeling GTPase signaling perturbations relevant to neurodevelopmental disorders. For additional product information or custom inquiries, please contact Ascent Research.
