The DOCK11 Knockout HEK293T Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population with targeted disruption of DOCK11 in HEK293T human embryonic kidney epithelial cells. This pool of cells harbors heterogeneous DOCK11 gene modifications, enabling loss-of-function studies without clonal selection, while effectively abrogating DOCK11 protein expression across the population.
The HEK293T host cell line, derived from human embryonic kidney epithelial cells, stably expresses SV40 large T-antigen for high transfection efficiency. These cells maintain epithelial characteristics such as barrier function and solute reabsorption, making them a robust platform for studying epithelial cell biology, signal transduction, and protein interactions.
DOCK11 functions as a GEF that activates Cdc42 by promoting GTP loading. Active Cdc42 triggers PAK1, WASP, and the Arp2/3 complex to drive actin polymerization and filopodia formation. DOCK11 responds to upstream signals from CXCR4 and integrin ??4??1 via PI3K and Rac1, and forms complexes with Elmo1 and Elmo2 to facilitate Cdc42 activation. Downstream, Cdc42 signaling modulates LIMK and cofilin to regulate actin dynamics, while SRF mediates transcriptional responses sustaining cytoskeletal remodeling and cell migration.
In HEK293T epithelial cells, DOCK11 knockout disrupts Cdc42-mediated actin remodeling, impairing migration and adherens junctions. This model enables dissection of the DOCK11?CCdc42?CPAK1 axis in epithelial barrier function and migratory responses, and provides a relevant system to explore DOCK11’s role in immunodeficiency, inflammatory diseases, and autoimmunity. The polyclonal population’s heterogeneity offers a representative model for phenotypic screening.
Applications include wound healing and Transwell migration assays to assess motility, immunofluorescence for F-actin to visualize cytoskeletal architecture, and western blotting for phospho-PAK1 as a pathway readout. Active Cdc42 pull-downs and co-immunoprecipitation studies can probe DOCK11 interactions with Elmo1/2 and downstream effectors. These assays support investigations of DOCK11 function in epithelial and immune contexts, as well as compound screening targeting DOCK11?CCdc42 signaling. For further information, please contact Ascent Research.
