Ptprk, Protein Tyrosine Phosphatase Receptor Type K, is a receptor tyrosine phosphatase. It is involved in regulating growth factor signalling, cell-cell adhesion, and acts as a potential tumour suppressor. It is associated with multiple pathways such as Wnt signalling and is important in various biological processes like cell proliferation, migration, and differentiation [2,3,4,5]. Genetic models, especially KO mouse models, are valuable in studying its functions.

In obesity-related studies, high-fat-fed PTPRK knockout male and female mice have lower weight gain and reduced hepatic fat accumulation. PTPRK was found to regulate glycolysis and de novo lipogenesis in hepatocytes, with its induced glycolysis enhancing PPARγ and lipogenesis [1]. In colorectal cancer, PTPRK knockout mouse models and xenografts confirm its role as a tumour suppressor, regulating growth factor and adhesion signalling, and suppressing epithelial to mesenchymal transition (EMT) in a catalysis-independent manner [2]. In colon cancer cells, knockdown of PTPRK potentiates the pro-oncogenic CD133-AKT pathway, reducing sensitivity to oxaliplatin [3].

In conclusion, Ptprk plays essential roles in metabolic regulation, intestinal repair, and tumour suppression. The use of Ptprk KO mouse models has provided valuable insights into its functions in obesity-associated metabolic diseases and cancer, highlighting its potential as a therapeutic target in these disease areas.