The DVL3 Knockout HEK293T Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population designed for advanced biomedical research on Wnt signal transduction. This product features targeted disruption of the human DVL3 gene in HEK293T cells, creating a loss-of-function model that avoids clonal selection biases. The polyclonal format captures a heterogeneous pool of edited cells, providing a robust genetic background for functional studies.
The host cell line, HEK293T, is a human embryonic kidney epithelial line stably expressing the SV40 large T antigen. This immortalized line is renowned for its high transfection efficiency and capacity for exogenous protein production, making it a standard platform in molecular and cellular biology. HEK293T cells are particularly suitable for Wnt pathway analysis due to their active signaling landscape and ease of genetic manipulation.
DVL3 encodes a cytoplasmic phosphoprotein that acts as a central scaffold in both canonical and non-canonical Wnt signaling. Upon Wnt ligand (e.g., WNT3A, WNT5A) binding to Frizzled receptors and LRP5/6 co-receptors, DVL3 is recruited to the membrane, where it undergoes phosphorylation by CK1 and polymerizes. This inhibits the ??-catenin destruction complex, composed of AXIN, APC, and GSK3??, leading to ??-catenin stabilization and nuclear translocation. In the nucleus, ??-catenin partners with TCF/LEF transcription factors to promote expression of targets such as AXIN2 and MYC. Concurrently, DVL3 mediates non-canonical pathways by activating Rho GTPases and JNK, influencing planar cell polarity and cytoskeletal reorganization. DVL3 interacts directly with AXIN1, APC, and CK1?? and is functionally linked to DVL1 and DVL2.
In the HEK293T background, DVL3 disruption allows unambiguous dissection of Wnt pathway contributions. The cell line??s endogenous Wnt activity makes the consequences of DVL3 loss readily apparent, enabling researchers to distinguish ??-catenin-dependent transcriptional outputs from non-canonical effects on migration and morphology. This polyclonal knockout model therefore serves as a precise tool to map DVL3??s role at the branch point of Wnt signaling without confounds from clonal adaptation.
Researchers can deploy these cells for mechanistic studies of Wnt-driven proliferation, metastasis, and drug resistance in cancer models, including colorectal, lung, and breast cancers. Functional genomics screens and target validation for Wnt inhibitors also benefit from this defined genetic background. Representative experimental approaches include Western blotting for DVL3 and ??-catenin, TOPFlash/FOPFlash dual-luciferase reporter assays, RT-qPCR for Wnt target genes, and immunofluorescence to visualize DVL3 puncta. Co-immunoprecipitation with AXIN and cell migration assays further probe protein interactions and non-canonical signaling. The model is equally applicable to neurodevelopmental disorder investigations and Alzheimer??s disease-related Wnt dysregulation. For detailed product information and technical support, please contact Ascent Research.
