The DNMBP Knockout A2780 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Homo sapiens A2780 ovarian carcinoma cell line, specifically engineered for loss-of-function studies of the DNMBP gene. This product provides a heterogeneous pool of gene-disrupted cells, enabling robust and reproducible functional analysis without the need for clonal selection or single-cell expansion. The polyclonal format preserves biological variability and facilitates assessment of DNMBP-dependent phenotypes in a physiologically relevant epithelial cancer model.
The A2780 cell line is an epithelial ovarian carcinoma model established from an untreated patient, commonly employed in high-grade serous ovarian cancer research. These cells maintain key epithelial characteristics, including E-cadherin?Cmediated cell?Ccell adhesion and responsiveness to platinum-based chemotherapeutic agents. Their well-documented signaling networks and tumorigenic properties make A2780 a suitable host for dissecting the molecular mechanisms that govern ovarian cancer progression, metastasis, and drug resistance.
DNMBP (also known as Tuba) encodes a multidomain scaffold protein that physically couples the large GTPase dynamin-1 and dynamin-2 to the cortical actin cytoskeleton and acts as a guanine nucleotide exchange factor (GEF) for the small Rho GTPase Cdc42. Through integrin-mediated adhesion and growth factor stimulation, upstream Src family kinases promote DNMBP-mediated localized activation of Cdc42 at cell?Ccell junctions. This triggers a signaling cascade involving the p21-activated kinase PAK1 and the actin nucleation-promoting factor N-WASP, which together drive Arp2/3 complex?Cdependent branched actin polymerization. Concurrently, DNMBP interacts directly with adherens junction components E-cadherin and ??-catenin, thereby integrating dynamin-dependent endocytosis with cytoskeletal remodeling to regulate junctional stability and cell migration.
In the A2780 ovarian carcinoma background, targeted disruption of DNMBP is anticipated to impair Cdc42-driven actin dynamics and adherens junction integrity, leading to defects in cell migration, adhesion, and receptor-mediated endocytosis. Given the established roles of cytoskeletal reorganization and junctional plasticity in ovarian cancer cell dissemination and peritoneal metastasis, this knockout model offers a physiologically pertinent system for investigating how DNMBP contributes to metastatic behavior and epithelial phenotype maintenance. Additionally, DNMBP has been linked to other pathologies such as Alzheimer??s disease and neurodevelopmental disorders, suggesting broader applicability of this model in understanding Cdc42-related signaling.
These polyclonal knockout cells are suited for a wide array of functional assays to probe metastatic potential, including quantitative transwell migration and Matrigel invasion assays, as well as cell?Cmatrix adhesion studies. Endocytic activity can be assessed using transferrin uptake measurements, while Cdc42 activation levels are readily monitored by PAK-PBD pull-down assays. The cells are also amenable to detailed immunofluorescence analysis of actin cytoskeleton organization and E-cadherin/??-catenin junctional localization, phospho-signaling profiling via western blot or multiplex approaches, and global transcriptomic analysis by RNA-seq. Furthermore, these cells provide a valuable platform for drug sensitivity screening to identify synthetic lethal interactions or to evaluate inhibitors targeting the DNMBP-Cdc42 interface. For additional information or to place an order, please contact Ascent Research.
