The DOCK11 Knockout HT29 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HT29 human colorectal adenocarcinoma cell line through CRISPR/Cas9-mediated disruption of the DOCK11 gene. This heterogeneous knockout pool provides a loss-of-function model for studying DOCK11-dependent biological processes without the limitations of clonal selection. The polyclonal format preserves the functional diversity of CRISPR editing outcomes, enabling robust and reproducible experiments in a population context.
The HT29 host cell line is a well-characterized human colorectal adenocarcinoma epithelial model isolated from a primary colon tumor. HT29 cells exhibit epithelial morphology and carry mutations in tumor suppressor genes including TP53 and APC, recapitulating key features of colorectal cancer biology. Widely used in studies of colon cancer progression, intestinal barrier integrity, and drug absorption, HT29 cells can differentiate into polarized enterocyte-like cells under specific culture conditions, making them suitable for investigations of epithelial permeability and transport mechanisms.
DOCK11 encodes a guanine nucleotide exchange factor (GEF) that specifically activates the Rho GTPase Cdc42. In response to upstream signals from receptor tyrosine kinases, integrins, cytokine receptors, or PI3K, DOCK11 facilitates GTP loading onto Cdc42. Active GTP-bound Cdc42 triggers downstream pathways involving PAK1, WASP, and the Arp2/3 complex, culminating in actin polymerization, filopodia formation, and regulation of cell migration and adhesion. DOCK11 also interacts with phosphoinositides and potentially CRK family proteins, integrating lipid signaling with cytoskeletal remodeling.
In the context of HT29 colorectal cancer cells, DOCK11 disruption provides a powerful tool to dissect Cdc42-driven processes that govern tumor cell motility, invasion, and epithelial barrier function. Given DOCK11’s role in immune cells and its association with autoimmune lymphoproliferative syndrome and early-onset autoimmunity, this knockout model also supports research at the interface of cancer immunology and autoimmune pathologies. The polyclonal population captures the spectrum of CRISPR-induced mutations, offering a balanced representation of loss-of-function effects.
Researchers can use this knockout model to interrogate Rho GTPase signaling in colorectal cancer, performing transwell migration and invasion assays, Cdc42 activation pull-down experiments, and immunofluorescence analysis of F-actin and filopodia. Barrier function studies employing TEER measurements and permeability assays are feasible due to the epithelial nature of HT29 cells. Additional applications include drug screening for Cdc42 inhibitors and immunoblotting for phosphorylated PAK1 or cofilin. For technical inquiries and ordering information, please contact Ascent Research.
