The DVL3 Knockout Raji Polyclonal Cells are a polyclonal population of Raji B lymphocytes in which the DVL3 gene has been disrupted using CRISPR/Cas9-mediated gene editing. This polyclonal knockout cell product provides a heterogeneous loss-of-function model suitable for investigating DVL3-dependent signaling and cellular functions without clonal selection bias. The cells are supplied as a ready-to-use polyclonal pool, enabling researchers to evaluate the overall impact of DVL3 disruption across a genetically diverse cell background.
The Raji cell line is a human B lymphocyte line originally derived from a Burkitt lymphoma patient. As a lymphoblastoid cell line, Raji cells maintain key features of B-cell biology, including surface immunoglobulin expression and the capacity to secrete antibodies, making them a widely used model for adaptive immunity and B-cell malignancies. Their transformed phenotype and rapid growth enable robust experimental manipulation, and they are commonly employed in studies of lymphoma biology, signal transduction, and drug response.
DVL3 encodes a cytoplasmic scaffold protein that plays a central role in transducing Wnt signals from Frizzled receptors. Upon activation by upstream regulators such as Wnt3a and Wnt5a ligands, DVL3 is phosphorylated by CK1?? and PAR1, promoting its interaction with the Axin complex, including APC and GSK3??. In canonical Wnt/??-catenin signaling, DVL3 inhibits the ??-catenin destruction complex, leading to stabilization and nuclear accumulation of ??-catenin, which partners with TCF/LEF transcription factors to drive expression of target genes like CCND1 and MYC. In non-canonical pathways, DVL3 modulates RhoA, Rac1, and JNK to regulate planar cell polarity and calcium flux. The protein also interacts with Dapper and Frizzled receptors, integrating multiple Wnt-dependent cellular responses.
In the Raji B-cell context, DVL3 knockout disrupts both canonical and non-canonical Wnt pathways, potentially impairing ??-catenin-dependent transcription and Rho/Rac-mediated cytoskeletal dynamics. Given the oncogenic role of Wnt signaling in Burkitt lymphoma and other B-cell malignancies, DVL3 loss-of-function may attenuate proliferation and survival signals, making this polyclonal knockout model valuable for dissecting Wnt-driven mechanisms in lymphomagenesis. Researchers can use these cells to explore how DVL3 contributes to MYC overexpression and CCND1 regulation, or to assess pathway crosstalk with other oncogenic drivers.
Typical applications include cellular phenotyping by Western blotting for DVL3 protein levels, RT-qPCR to confirm mRNA disruption, and ??-catenin reporter assays to measure Wnt pathway activity. Functional studies may employ cell proliferation assays, apoptosis assays (e.g., Annexin V staining), and drug sensitivity screening to evaluate responses to Wnt inhibitors or chemotherapeutic agents. The polyclonal nature of the knockout population allows for assessment of heterogeneous cellular responses, making it suitable for pooled screening approaches. For further details, please contact Ascent Research.
