Protein tyrosine phosphatase receptor type J (PTPRJ) is a tumour suppressor that has been implicated in several signalling pathways including cell proliferation, differentiation, adhesion and immune cell activation. Its expression in various cell types including endothelial, epithelial and haematopoietic cells is known, however to date there is little information on its expression in keratinocytes and melanocytes. This is despite the fact that skin cancers are the most common cancer worldwide. Immunofluorescence, quantitative RT-PCR and Western blotting were used to examine PTPRJ in keratinocytes and melanocytes. A number of bioinformatic tools were also used to analyse the gene to identify any the enhancer and promoter regions of PTPRJ and any alternative splicing events. Results from this study show that keratinocytes (HaCaT) express PTPRJ, with localisation patterns around the cell periphery, possibly in membrane ruffles and podosome-like structures. CAGE data from ENCODE and FANTOM5 suggest that there is cell type-specific expression of PTPRJ, with chromatin states indicating differential activation of two promoter and enhancer regions at this locus. These datasets also reveal the presence of multiple isoforms of PTPRJ, including transcripts with splicing events that give rise to truncated transcripts and alternative 3’UTRs. Putative proteins encoded by these transcripts include possible dominant-negative decoy receptors (Isoforms 2, 3, 4 and 6), as well as a protein lacking the signal sequence of full-length PTPRJ (Isoform 4). The expression of Isoform 4 was of particular interest due to the relatively high number of CAGE peaks seen in melanocytes, with little to no expression in other cell types. qRT-PCR was able to confirm the presence of this transcript in melanocytes for the first time, with quantitative data corroborating bioinformatic predictions. A quantitative assay was also developed for use in wound healing experiments to investigate the function of PTPRJ in HaCaT cell migration. Using this in vitro wound healing model, we found that antibodies against PTPRJ prevented the ability of HaCat cells to close the “wound”, suggesting that PTPRJ signalling is necessary for keratinocyte migration at the wound edge. Modulation of this signalling pathway may be a useful modality for treating wounds in a clinical setting.