Abstract
Pemphigus vulgaris (PV) is a life-threatening autoimmune mucocutaneous blistering disease. We previously showed that a genetic variant within the ST18 promoter promotes ST18 up-regulation in a p53/p63-dependent manner and is associated with a 6-fold increased risk to develop PV. ST18 was also found to be overexpressed in the skin of PV patients. In addition, it has been shown that desmoglein 3 (DSG3) down-regulation is associated with increased p53 expression and activity. Based on these data, using a combination of reporter assays, Western blotting, confocal immunofluorescence microscopy, we investigated the possibility that ST18, DSG3 and p53 may be jointly involved on the pathogenesis of PV.
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