DVL2 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population, generated by disruption of the DVL2 gene in the Jurkat T-lymphocyte background. This pooled population provides a physiologically relevant loss-of-function model for studying DVL2-dependent signaling without the clonal biases inherent in single-cell-derived lines.
The Jurkat cell line originates from an acute T cell leukemia patient and represents an immortalized human T lymphocyte model widely employed in immunology and oncology research. These cells retain key features of T-cell biology, including antigen receptor-mediated activation, cytokine secretion, and reliance on specific signal transduction networks for survival and proliferation.
DVL2 (Dishevelled 2) is a central scaffold protein in Wnt signaling, relaying signals from Frizzled receptors to multiple downstream pathways. It participates in the canonical Wnt/??-catenin axis, where it inhibits the destruction complex (comprising Axin, APC, and GSK-3??) to stabilize ??-catenin and enable TCF/LEF-mediated transcription. DVL2 also mediates non-canonical planar cell polarity and calcium pathways, regulating RhoA, Rac1, JNK, and NFAT. Its function is modulated by phosphorylation from kinases such as CK1, CK2, and PKC, and by interactions with partners like Axin, Dapper, and Van Gogh.
In Jurkat cells, DVL2 integrates Wnt cues that influence T-cell activation, proliferation, and potentially leukemogenic programs. Disruption of DVL2 abrogates both ??-catenin-driven gene expression (e.g., MYC, CCND1) and ??-catenin-independent signaling cascades, impairing downstream effectors like AP-1 and NFAT. This knockout model thus enables dissection of DVL2-specific contributions to T-ALL pathogenesis and normal T-cell function, revealing dependencies on Wnt pathway branches.
Researchers can employ these polyclonal knockout cells in a broad spectrum of functional assays, including TopFlash reporter assays for ??-catenin activity, RT-qPCR of Wnt target genes, Western blotting for pathway components, co-immunoprecipitation to map DVL2 interactomes, phospho-signaling analyses (e.g., JNK activation), and flow cytometry-based cell cycle and apoptosis studies. Additionally, the cells are suitable for Wnt pathway modulator screening and migration assays to explore non-canonical signaling roles. For further information, please contact Ascent Research.
