Anti-Desmoglein-2 Antibody

Rabbit polyclonal antibodies raised against Desmoglein-2 (DSG2) provide researchers with a specific reagent for studying desmosomal adhesion in epithelial and cardiac tissue. This unconjugated primary antibody, supplied by Antibodies.com in a 100 µl vial, is validated for Western blot (WB) and immunohistochemistry (IHC) applications on human samples. The polyclonal format means the reagent can recognize multiple epitopes across the DSG2 extracellular and cytoplasmic domains, which can help when signal strength from a monoclonal reagent is insufficient.

DSG2 is a calcium-dependent transmembrane cadherin and a core structural component of desmosomes, the intercellular junctions that anchor intermediate filaments at sites of strong tissue adhesion. It is widely expressed in simple and stratified epithelia, as well as in cardiomyocytes, where it works alongside desmocollin-2, plakoglobin, plakophilin-2, and desmoplakin to maintain mechanical coupling between adjacent cells. Loss-of-function mutations in DSG2 are a recognized genetic cause of arrhythmogenic right ventricular cardiomyopathy (ARVC), and reduced DSG2 expression has been reported in several epithelial cancers, making the target relevant to both cardiovascular and oncology research.

For Western blot, the antibody can be used to confirm full-length DSG2, which migrates near 160 kDa in reducing gels, and to compare expression between normal and disease tissue lysates. In IHC, it produces membrane-localized staining at cell-cell borders in formalin-fixed paraffin-embedded sections, consistent with desmosomal localization in epidermis and myocardium. Because the reagent is unconjugated, researchers can pair it with HRP-, biotin-, or fluorophore-conjugated secondary antibodies according to their detection chemistry. The antibody is supplied as a 100 µl liquid format; for long-term use, store frozen at -20 °C in working aliquots to limit freeze-thaw cycles, and protect from light if a fluorophore-conjugated secondary is later selected.