The DVL2 Knockout Raji Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human Raji B lymphocyte line, engineered for loss-of-function studies of the DVL2 gene. This polyclonal pool harbors heterogeneous CRISPR/Cas9-mediated disruptions of the endogenous DVL2 locus, providing a genetically diverse model for interrogating Wnt signal transduction. By ablating DVL2 expression across a mixed cell population, researchers can assess the overall impact on canonical and non-canonical Wnt pathways without clonal biases, enabling robust functional genomics and drug discovery applications in a lymphoma context.
The Raji host cell line is a well-characterized human lymphoblastoid line established from a Burkitt’s lymphoma patient. As a B lymphocyte model, Raji cells are extensively employed in immunology and cancer research, particularly for studying B cell malignancies, adaptive immunity, and oncogenic transformation driven by aberrant signaling networks. Their rapid proliferation and defined genetic background make them an ideal platform for investigating the molecular underpinnings of lymphoma biology and for high-throughput screening of targeted therapeutics.
DVL2 (Dishevelled 2) is a cytoplasmic scaffold protein that serves as a central relay hub in Wnt signaling cascades. In the canonical Wnt/??-catenin pathway, DVL2 is activated by Frizzled receptors upon binding of Wnt ligands such as Wnt3a; it then recruits the ??-catenin destruction complex??comprising Axin, APC, GSK3??, and CK1??to the receptor complex, leading to inhibition of ??-catenin degradation. Stabilized ??-catenin translocates to the nucleus and promotes TCF/LEF-dependent transcription of target genes including c-Myc (MYC) and Cyclin D1 (CCND1). DVL2 also engages non-canonical pathways by modulating RhoA and Rac1 GTPases and the JNK kinase cascade, thereby influencing planar cell polarity and cytoskeletal remodeling.
In the Raji Burkitt’s lymphoma background, DVL2-mediated Wnt signaling is implicated in cell proliferation, survival, and chemoresistance. Disruption of DVL2 in this model allows dissection of its contribution to B cell lymphomagenesis and immune cell function, particularly with respect to ??-catenin stabilization and downstream oncogenic transcriptional programs. The engineered knockout model enables direct assessment of DVL2 dependency in a lymphoma context, facilitating exploration of synthetic lethal interactions and pathway-targeted strategies for hematologic malignancies.
Typical research applications include functional analysis of canonical Wnt/??-catenin signaling in B cell lymphoma, investigation of DVL2-dependent proliferation and apoptosis using flow cytometry, identification of DVL2-mediated drug resistance mechanisms, and genome-wide CRISPR screens for Wnt pathway modifiers. Representative assays encompass western blotting for DVL2 and ??-catenin, RT-qPCR quantitation of Wnt target genes (c-Myc, CCND1, AXIN2), TCF/LEF luciferase reporter assays, co-immunoprecipitation of DVL2 with Frizzled or Axin, and phospho-DVL2 analysis. For further information, please contact Ascent Research.
