DOCK4 Knockout MES-OV Polyclonal Cells comprise a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Mus musculus MES-OV ovarian surface epithelial cell line. This product features targeted disruption of the DOCK4 gene, generating a heterogeneous pool of cells with loss-of-function mutations that ablate functional DOCK4 protein expression. By leveraging a non-clonal, polyclonal knockout format, the cell population provides a robust model for studying DOCK4-dependent biological processes while mitigating clonal selection artifacts. The knockout pool preserves the diversity of editing outcomes, enabling experiments that require population-level phenotypic assessment without the bias associated with monoclonal derivatives.
MES-OV cells are immortalized mouse ovarian surface epithelial cells widely employed as a model for ovarian surface epithelial cell biology and malignant transformation. Derived from normal ovarian surface epithelium, MES-OV cells retain key epithelial characteristics and respond to oncogenic stimuli, making them particularly relevant for investigating early events in ovarian carcinogenesis. Their well-characterized signaling landscape and tractability for functional genomics render them an ideal host for dissecting molecular pathways that drive ovarian cancer initiation and progression, especially those involving cytoskeletal reorganization and cell motility.
DOCK4 encodes a guanine nucleotide exchange factor (GEF) that specifically activates RAC1 by catalyzing the exchange of GDP for GTP. DOCK4 often forms a functional complex with ELMO1 or ELMO2, which together facilitate RAC1-GTP loading and subsequent downstream signaling. Activated RAC1-GTP engages effectors such as PAK1/2/3 and JNK, and promotes actin cytoskeleton reorganization through the LIMK-cofilin pathway. Phosphorylation of cofilin by LIMK inhibits its actin-severing activity, leading to stabilization of filamentous F-actin, lamellipodia formation, and enhanced cell migration and invasion. Upstream regulators of DOCK4 include integrin receptors, platelet-derived growth factor (PDGF), and WNT ligands, which stimulate DOCK4-mediated RAC1 activation in response to extracellular cues.
In the context of ovarian surface epithelial cells, DOCK4-dependent RAC1 signaling is critically implicated in the regulation of actin dynamics, cell adhesion, and invasive potential??processes frequently dysregulated during ovarian cancer metastasis. The DOCK4 Knockout MES-OV Polyclonal Cells provide a physiologically relevant loss-of-function platform to decipher DOCK4??s role in these processes. By eliminating DOCK4 expression, researchers can interrogate how its absence alters RAC1-GTP levels, actin polymerization, and migratory behavior in a cell type directly linked to ovarian cancer. This model is thus instrumental for dissecting the molecular underpinnings of DOCK4-driven protrusion dynamics and for evaluating therapeutic targets within the DOCK4-ELMO-RAC1 axis.
Typical research applications utilizing this knockout model include quantitative assessment of RAC1-GTP pull-down, western blotting for DOCK4 and phospho-PAK, wound healing migration assays, transwell invasion assays, immunofluorescence staining for F-actin, and live-cell imaging of lamellipodial protrusion dynamics. The polyclonal pool is ideally suited for functional genomics studies, small molecule inhibitor screening targeting the DOCK4-ELMO interaction, and pathway dissection in ovarian cancer models. These cells enable systematic exploration of how DOCK4 disruption impacts cell motility and cytoskeletal organization at the population level. For further technical information, please contact Ascent Research.
