Ptprd, also known as receptor-type protein tyrosine phosphatase, receptor type D, likely functions as a neuronal cell adhesion molecule and synaptic specifier. It is involved in multiple signaling pathways, such as the JAK-STAT pathway, and plays a crucial role in various biological processes related to the nervous system. Its study through genetic models can provide insights into its function and its implications in disease [1].

In mouse models, genetic ablation of Ptprd leads to a strong loss of appetite, leanness, and an inability to respond to the orexigenic effects of asprosin, indicating its role in regulating appetite. Ablation of Ptprd specifically in AgRP neurons causes resistance to diet-induced obesity [4].

In oligodendrogliomas, focal chromosomal rearrangements in PTPRD with associated decreased gene expression were observed in relapsed tumors, and low PTPRD expression was associated with poor overall survival in the TCGA diffuse glioma cohort, suggesting its potential as a marker of tumor aggressiveness [2].

In hepatocellular carcinoma, PTPRD is a down-regulated tumor-suppressor gene involved in tumor progression, migration, apoptosis, invasion, and immune suppression through multiple signaling pathways [3].

In conclusion, Ptprd is essential in regulating neuronal functions, appetite, and is involved in cancer-related processes. Mouse models with Ptprd knockout or conditional knockout have been instrumental in revealing its role in obesity-related phenotypes and cancer, highlighting its potential as a therapeutic target in these disease areas.