The DSC2 Knockout HeLa Polyclonal Cells are a CRISPR/Cas9-edited polyclonal cell population derived from HeLa cells, featuring disruption of the DSC2 gene that encodes desmocollin 2. This polyclonal knockout product provides a heterogeneous mix of cells each carrying a CRISPR/Cas9-mediated loss-of-function modification, eliminating functional DSC2 protein and enabling detailed study of desmosomal adhesion without clone-specific artifacts.
HeLa cells are an immortalized epithelial line from cervical adenocarcinoma, widely employed as a model for epithelial biology, cancer research, and drug discovery. Their robust growth and well-documented characteristics make them an ideal platform for generating knockout populations to investigate cell adhesion and signaling mechanisms.
DSC2 is a desmosomal cadherin that forms calcium-dependent adhesive interactions with desmoglein 2 (DSG2) and links to the intermediate filament cytoskeleton via plakoglobin (JUP), desmoplakin (DSP), and plakophilins (PKP2, PKP3). Regulated by TP63, calcium, retinoid signaling, and EGFR, DSC2 influences the stability of desmosomal complexes and may modulate Wnt/??-catenin signaling by controlling plakoglobin??s nuclear availability. Disruption of DSC2 in this model impairs desmosome assembly, compromising cell?Ccell adhesion and potentially altering proliferative and migratory signaling.
In HeLa cells, DSC2 knockout disrupts epithelial barrier integrity and enhances migratory capacity, recapitulating aspects of malignant progression. This model is instrumental for dissecting how desmosomal defects contribute to cancer metastasis and for mimicking pathogenic mechanisms of DSC2-related diseases such as arrhythmogenic right ventricular cardiomyopathy and skin fragility disorders.
Researchers can utilize this knockout population for immunofluorescence localization of desmosomal components, cell aggregation assays, and TEER-based barrier function measurements. It also supports transwell migration/invasion assays, drug screening for cadherin modulators, and expression profiling via RT-qPCR or Western blotting. For further information, please contact Ascent Research.
