Ptprg, short for Protein Tyrosine Phosphatase Receptor Type G, is known to interact with and regulate several tyrosine kinases, exerting a tumor suppressor role in several types of cancers [2]. It contains a carbonic anhydrase-like domain (CAH) and a fibronectin type III domain in the N-terminal portion, which are associated with its role as a [HCO3-] sensor in vascular and renal tissues and a possible interaction domain for cell adhesion, respectively [2].

In Alzheimer's disease (AD), single-cell and spatial transcriptomics revealed that microglia subpopulation Mic_PTPRG can communicate with specific neurons, causing them to express PTPRG [1]. Within neurons, PTPRG binds and upregulates the m6A methyltransferase VIRMA, inhibiting translation of PRKN mRNA to block mitophagy-mediated neuronal death [1]. Also, in nasopharyngeal carcinoma, PTPRG suppresses tumor growth and invasion via inhibition of Akt signaling, with EGFR as a potential interacting partner [3].

In conclusion, Ptprg has diverse functions in different biological processes and diseases. In AD, it modulates a pathway related to neuronal death, and in nasopharyngeal carcinoma, it acts as a tumor suppressor through inhibiting a key signaling pathway. Studies using various models help to understand these functions, providing insights into disease mechanisms and potential therapeutic targets.