The DIP2A Knockout MES-OV Polyclonal Cells product is a CRISPR/Cas9-edited polyclonal knockout cell population derived from the MES-OV mouse embryonic stem cell line. This loss-of-function model disrupts the Disco-interacting protein 2 homolog A (DIP2A) gene, providing a powerful tool for investigating DIP2A-dependent signaling in pluripotent stem cell biology. The polyclonal format captures a heterogeneous pool of knockout alleles generated by CRISPR/Cas9-mediated gene disruption, enabling studies that do not rely on clonal homogeneity. This product is designed for researchers examining the molecular mechanisms underlying cell migration, differentiation, and tumor suppression.
The MES-OV cell line is a well-characterized mouse embryonic stem cell model established from the 129/Sv strain. These pluripotent cells maintain the capacity to differentiate into derivatives of all three germ layers, making them an ideal platform for exploring early development and lineage commitment. MES-OV cells express key pluripotency factors and respond to differentiation cues, providing a physiologically relevant context for dissecting the roles of genes like DIP2A in maintaining stemness versus initiating differentiation programs. Their robust growth and genetic tractability facilitate efficient CRISPR/Cas9 editing and downstream functional assays.
DIP2A functions as a receptor/adaptor protein within the netrin-1/DCC signaling axis. Mechanistically, DIP2A interacts with DCC, NEO1, UNC5A, and DLG4 to transduce signals from the ligand netrin-1 (NTN1). Downstream, DIP2A modulates the activity of ERK1/2 (MAPK3/1), RHOA, RAC1, and CTNNB1, thereby influencing cytoskeletal dynamics, cell migration, and epithelial-mesenchymal transition (EMT). The gene is regulated upstream by miR-125b, TGFB1, SOX2, and WNT3A, placing DIP2A at the crossroads of critical morphogenetic and oncogenic pathways. Its involvement in Rho GTPase and Wnt signaling further underscores its role in coordinating cell polarity and movement.
In the context of MES-OV pluripotent stem cells, DIP2A knockout is predicted to impair netrin-1/DCC-mediated signaling, leading to altered MAPK and Rho GTPase activities. This perturbation can disrupt the delicate balance between self-renewal and differentiation, potentially affecting the expression of pluripotency markers and lineage-specific transcription factors. The polyclonal knockout population allows researchers to assess the collective impact of DIP2A loss on early developmental processes, such as germ layer specification and migratory behavior, without the artifacts of clonal selection. Such a model is invaluable for studying how DIP2A integrates extrinsic cues to regulate cell fate decisions.
This product is ideally suited for a wide range of applications in cancer metastasis research, stem cell differentiation studies, and neurodevelopmental disease modeling. Representative assays include Western blotting to confirm DIP2A depletion and monitor pluripotency markers, RT-qPCR for gene expression profiling, immunofluorescence to visualize cell morphology, scratch wound migration assays to quantify motility, embryoid body formation to assess differentiation potential, and RNA-seq for transcriptome-wide analysis. By employing these techniques, researchers can elucidate DIP2A??s role in migration and invasion, screen for modifiers of the pathway, or model aspects of intellectual disability. For additional information or technical support, please contact Ascent Research.
