DOCK11 Knockout HeLa Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population designed to disrupt the expression of the DOCK11 gene. This loss-of-function model is generated in the HeLa cell line and provides a heterogeneous pool of edited cells, enabling the study of DOCK11-dependent processes without clonal selection artefacts. The knockout cells are suitable for a wide range of functional assays to probe the roles of DOCK11 in actin cytoskeletal dynamics, cell migration, and signal transduction downstream of immune and cancer-associated pathways.
The HeLa cell line is an immortalized epithelial cell line derived from a cervical adenocarcinoma, and it is positive for human papillomavirus 18 (HPV18). As one of the most widely used human cancer cell lines, HeLa offers a robust and well-characterized model system for studying oncogenic signaling, cell motility, and host-pathogen interactions. Its adherent growth and high transfectability facilitate many cell-based assays, making it an advantageous host for generating knockout models of genes involved in cytoskeletal regulation and disease-associated pathways.
DOCK11 (dedicator of cytokinesis 11) is a guanine nucleotide exchange factor (GEF) that specifically activates the Rho GTPases CDC42 and RAC1, promoting actin polymerization and cytoskeletal reorganization. Its activity is stimulated by B-cell receptor activation, SRC family kinases, and PI3K, and it cooperates with ELMO1/2 adaptor proteins and PIP3 to modulate downstream effectors such as PAK1, the WASP/WAVE complex, and LIMK. Through these interactions, DOCK11 controls cofilin-mediated actin dynamics, facilitating cell migration and adhesion. In immune cells, DOCK11 is essential for B-cell receptor signaling and platelet activation, linking its GEF activity to combined immunodeficiency and autoinflammatory disorders.
In HeLa cells, DOCK11 disruption offers a valuable tool to dissect its contribution to actin-based motility and invasion programs that are often dysregulated in cancer. Although HeLa cells are not of immune origin, they retain core machinery for Rho GTPase signaling, allowing researchers to investigate how DOCK11-dependent CDC42/RAC1 activation affects cell migration, proliferation, and morphology. Moreover, the knockout model can be used to explore the cross-talk between HPV18 oncoproteins and the host cytoskeleton, and to evaluate the therapeutic potential of targeting DOCK11-GEF activity in cervical carcinoma and other epithelial cancers.
These knockout cells are ideal for western blotting and RT-qPCR to confirm DOCK11 loss, immunofluorescence to visualize actin changes, and cell migration assays (wound healing, transwell) to assess functional consequences. Flow cytometry, co-immunoprecipitation, GTPase pull-downs, and phospho-signaling analyses can map DOCK11 networks and downstream events. Applications span immunology, cancer biology, hematopoiesis, immunodeficiency modeling, and drug target identification. For further details, contact Ascent Research.
