The DOCK7 Knockout HeLa Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human cervical carcinoma HeLa cell line. This product introduces a targeted disruption of the DOCK7 gene, generating a loss-of-function model for investigating the roles of DOCK7 in cellular signaling, cytoskeletal organization, and motility. The polyclonal format provides a heterogeneous pool of genotypes, reflecting the natural variability in gene editing outcomes, and is well-suited for functional studies where uniform knockout is not required.
HeLa cells are an immortalized epithelial cell line originally isolated from a cervical adenocarcinoma. They are extensively employed in cell biology, cancer research, and drug discovery due to their robust growth, ease of transfection, and well-characterized signaling pathways. As a model for epithelial-derived cancers, HeLa cells enable investigation of fundamental processes such as proliferation, apoptosis, migration, and signal transduction.
DOCK7 is a guanine nucleotide exchange factor (GEF) that specifically activates the small GTPases Rac1 and Cdc42, which are key regulators of the actin cytoskeleton. DOCK7 functions downstream of integrin signaling and growth factor receptors, interacting with ELMO1 and ELMO2 to catalyze nucleotide exchange on Rac1 and Cdc42. This activation triggers a signaling cascade involving PAK kinases, LIMK, and cofilin, leading to actin polymerization and cytoskeletal reorganization. Additionally, DOCK7-mediated signaling engages the JNK and p38 MAPK pathways. Consequently, DOCK7 knockout disrupts these pathways, impairing Rac1/Cdc42 activation and downstream cytoskeletal dynamics.
In the HeLa cellular context, disruption of DOCK7 is particularly relevant for studying epithelial cell migration, invasion, and adhesion, which are processes frequently dysregulated in cancer metastasis. DOCK7 has also been implicated in neurodevelopmental disorders and epileptic encephalopathy, and while HeLa cells are not neuronal, the conserved mechanisms of cytoskeletal regulation can provide insights into fundamental processes applicable to neurobiology. By eliminating DOCK7 function, this model permits the dissection of its specific contributions to actin-dependent motility and adhesion in an epithelial background.
This knockout cell product is suitable for a range of experimental applications, including cell migration assays (wound healing, transwell migration/invasion), Rho GTPase activation assays to measure Rac1 and Cdc42 activity, F-actin immunofluorescence for cytoskeletal visualization, Western blot analysis of DOCK7 and downstream effectors, and cell adhesion assays. The polyclonal knockout population serves as a valuable tool for investigating the molecular mechanisms of DOCK7 in cancer cell invasion, cytoskeletal dynamics, and drug screening efforts. For further assistance or custom inquiries, please contact Ascent Research.
