Receptor-type tyrosine-protein phosphatase epsilon (PTPRE) (PTPRE)

Receptor-type tyrosine-protein phosphatase epsilon (PTPRE) is a signaling enzyme that exists as both transmembrane (PTPeM) and cytoplasmic (PTPeC) isoforms, produced via alternative initiation and splicing (UniProt P23469). It acts as a physiological activator of Src family kinases in specific contexts, such as osteoclasts and breast cancer cells, while acting as a negative regulator of insulin receptor signaling in metabolic tissues (PubMed: 11035015, 21454524). In oncology, PTPRE is a known collaborator of the Neu/ErbB2 oncogene, and its inhibition has been shown to reduce tumor growth in preclinical models (PubMed: 10688914). In bone biology, PTPRE is essential for proper osteoclast adhesion and bone resorption, making it a potential target for antiresorptive therapy in osteoporosis (PubMed: 15107411). Therapeutic strategies targeting PTPRE include the development of small molecule phosphatase inhibitors and RNA-based approaches, such as siRNA, to degrade PTPRE mRNA and reduce protein expression. Despite its therapeutic potential, challenges remain due to the high structural homology among PTP family members and the dual role of PTPRE in different tissue types.

Other names

PTP epsilonR-PTP-epsilonProtein tyrosine phosphatase receptor type EHPTPEPTPE

RNA interference (RNAi) targeting PTPRE mRNA to reduce protein expression; inhibition of phosphatase catalytic activity to modulate signaling pathways such as Src/MAPK and PI3K/Akt.