The DSG2 Knockout HEK293T Polyclonal Cells product provides a CRISPR/Cas9-edited polyclonal knockout cell population targeting the DSG2 gene in the HEK293T background. This loss-of-function model enables systematic analysis of desmoglein-2 biology by disrupting its expression across a heterogeneous cell pool, circumventing clonal selection artifacts while retaining target-gene disruption via CRISPR/Cas9-mediated gene editing. The polyclonal format offers a robust platform for interrogating DSG2-dependent processes without the limitations of single-cell-derived clones.
HEK293T is a widely utilized immortalized human embryonic kidney epithelial cell line, derived from HEK293 cells through stable expression of the SV40 large T antigen. This modification permits episomal replication of plasmids containing the SV40 origin of replication, rendering the line highly amenable to transient transfection, recombinant protein expression, and lentiviral or retroviral vector production. The epithelial origin and robust transfectability of HEK293T cells make them a versatile chassis for dissecting gene function in a controlled in vitro setting.
Desmoglein-2 (DSG2) is a transmembrane cadherin of the desmosomal family that mediates strong calcium-dependent cell-cell adhesion. Mechanistically, DSG2 engages in homophilic trans-interactions at intercellular junctions, clustering and recruiting the armadillo protein plakoglobin (JUP) and the plakin family member desmoplakin (DSP), which together anchor intermediate filaments to the plasma membrane, thereby conferring mechanical resilience to epithelial sheets. DSG2 is regulated upstream by transcription factors p63, STAT3, GATA3, and GRHL2, and by calcium and epidermal growth factor (EGF) signaling. It interacts directly with desmosomal partners including plakophilin-2 (PKP2), plakophilin-3 (PKP3), desmocollin-2 (DSC2), and p120 catenin (CTNND1), and with the epidermal growth factor receptor (EGFR). Loss of DSG2 disrupts desmosome assembly, leading to junctional destabilization, cytoskeletal reorganization, and altered expression of epithelial-to-mesenchymal transition (EMT) markers such as vimentin and N-cadherin, as well as the cell cycle regulator cyclin D1.
In HEK293T cells, which retain core desmosomal components despite their transformed nature, DSG2 disruption provides a simplified yet physiologically relevant model to study desmosome dynamics. The polyclonal knockout population uncovers the breadth of cellular responses to DSG2 loss, including impaired adhesion, reduced epithelial barrier integrity, and activation of signaling cascades that promote a mesenchymal phenotype. This context is especially valuable for dissecting DSG2’s role in oncogenic EMT, where its loss is often observed in advanced gastric, breast, and colorectal cancers, and for modeling molecular aspects of arrhythmogenic right ventricular cardiomyopathy (ARVC), a disease frequently linked to desmosomal gene mutations.
The DSG2 Knockout HEK293T Polyclonal Cells are suited for a range of experimental applications, including mechanistic studies of desmosomal adhesion, high-content screening for compounds that restore cell adhesion, and detailed examination of EMT signaling pathways. Typical assays include Western blotting for DSG2 and associated proteins, immunofluorescence localization of desmosomal plaques, electric cell-substrate impedance sensing (ECIS) for barrier function, cell aggregation/adhesion assays, RT-qPCR profiling of EMT markers, and migration or invasion assays. For further information or custom requirements, please contact Ascent Research.
