The DMTN Knockout MES-OV Polyclonal Cells product comprises a population of human mesenchymal stromal cells in which the DMTN gene has been disrupted by CRISPR/Cas9-mediated genome editing. This polyclonal knockout model provides a heterogeneous cell pool with targeted loss of DMTN function, enabling robust investigation of dematin-dependent processes without clonal selection bias. The knockout is generated in the MES-OV host cell background, maintained in culture as a polyclonal population, and supplied as a ready-to-use reagent for functional genomics studies.
MES-OV is a human mesenchymal stromal cell line derived from ovarian tissue. These multipotent cells retain the capacity to differentiate into osteoblasts, chondrocytes, and adipocytes, and they actively support hematopoiesis and contribute to tissue repair. Their ovarian origin makes them particularly relevant for studies of ovarian physiology, stromal?Cepithelial interactions, and the tumor microenvironment. The MES-OV host system is well characterized for adhesion, migration, and cytoskeletal dynamics, making it an ideal platform to interrogate the role of actin-binding proteins such as DMTN.
DMTN (dematin) encodes an actin-bundling protein that crosslinks filamentous actin (ACTB) and interacts with spectrin family members SPTA1 and SPTB, as well as the adapter EBP41 (Band 4.1), to reinforce the cortical cytoskeleton. Phosphorylation by upstream kinases ABL1, ABL2, and SRC, often downstream of growth factor receptors such as EGFR and PDGFR, regulates DMTN activity. DMTN contributes to Rho GTPase-regulated cytoskeletal dynamics (CDC42, RAC1, RHOA), which in turn influence focal adhesion assembly through vinculin and FAK. Thus, loss of DMTN uncouples receptor signaling from actin remodeling, impairing cell adhesion and migration.
In MES-OV cells, DMTN knockout disrupts the cortical actin?Cspectrin scaffold, leading to profound changes in cell morphology, adhesion to extracellular matrix, and migration capacity. These mesenchymal stromal cells rely on cytoskeletal integrity for mechanotransduction, lineage specification, and paracrine functions. By eliminating DMTN, researchers can examine how loss of actin bundling and spectrin tethering affects osteogenic, chondrogenic, and adipogenic differentiation pathways. The ovarian derivation of the host line adds relevance for dissecting DMTN??s role in ovarian tissue homeostasis and stromal contributions to ovarian cancer metastasis.
This knockout model is suited for diverse experimental workflows, including wound healing and Transwell migration/invasion assays, adhesion assays on ECM components, and quantitative imaging of F-actin using phalloidin. It enables co-immunoprecipitation studies to map altered protein?Cprotein interactions (e.g., with ADD1, TPM1) and phospho-kinase profiling to assess signaling rewiring. Applications extend from fundamental research on cytoskeletal regulation in mesenchymal stem cells to translational studies on cancer metastasis, hereditary elliptocytosis, and pyropoikilocytosis. For additional product information, usage guidance, or custom generation services, please contact Ascent Research.
