The DSG2 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population from the Raji B lymphocyte line. The product uses CRISPR/Cas9-mediated gene disruption to generate a heterogeneous pool of DSG2 loss-of-function alleles, avoiding clonal bias. The polyclonal format preserves genetic diversity, suitable for population-level studies like drug response profiling. These cells are a versatile platform for investigating DSG2 in a suspension immune context.
The parental Raji cell line originates from a human Burkitt lymphoma and maintains an Epstein-Barr virus-positive phenotype, growing in suspension as mature B lymphocytes. Raji cells are widely adopted for their robust antibody production, antigen presentation capability, and adaptive immune response features. Their transformed state retains key signaling machinery, making them ideal for examining how desmosomal cadherins like DSG2 influence lymphocyte adhesion, survival, and communication. This background provides a physiologically relevant milieu beyond classical epithelial and cardiac tissues.
DSG2 encodes a calcium-dependent desmosomal cadherin that mediates homophilic adhesion and anchors intermediate filaments through plakoglobin and desmoplakin. It forms complexes with plakophilin, desmocollin, and keratin filaments, critical for tissue integrity. Transcription of DSG2 is driven by Wnt-responsive TCF/LEF factors and is modulated by p53 and interferon-gamma; additionally, protein kinase C phosphorylates its cytoplasmic domain. Upon knockout, desmosome disassembly frees plakoglobin, which can translocate to the nucleus and regulate ??-catenin/TCF transcriptional programs. Consequently, DSG2 loss connects adhesion disruption to altered Wnt/??-catenin signaling.
In Raji B lymphocytes, DSG2 knockout allows dissection of non-desmosomal cadherin functions. Although these suspension cells lack classical desmosomes, DSG2 may modulate Wnt/??-catenin activity, influencing proliferation, migration, or survival. This model is particularly valuable for pemphigus research, where anti-DSG2 autoantibodies cause adhesion loss, and for studying arrhythmogenic right ventricular cardiomyopathy mechanisms in a non-cardiac context. Furthermore, it aids in examining cadherin switching events during cancer metastasis and B lymphocyte adhesion-dependent signaling.
These polyclonal knockout cells are suitable for western blotting, immunofluorescence, and flow cytometry to verify DSG2 depletion. Cell aggregation and migration assays probe adhesion and motility, while Wnt reporter and co-immunoprecipitation examine signaling via plakoglobin and ??-catenin. Apoptosis assays extend utility to survival studies. Applications span cell adhesion, pemphigus autoimmunity, cancer metastasis, and B lymphocyte biology. For further details, contact Ascent Research.
