Dact2, also known as Dapper homolog 2, is a member of the DACT gene family. It plays crucial roles in tissue development and injury, and is involved in regulating intracellular signaling pathways, especially the Wnt/β -catenin and TGF -β signaling pathways. These pathways are fundamental in various biological processes, and Dact2's regulation of them is of great biological importance. Genetic models, such as zebrafish and mouse models, have been used to study Dact2 [1,2,3].

In a zebrafish Dact2 knockout model, the absence of Dact2 enhanced the expression of genes related to tumor invasion, migration, and epithelial-mesenchymal transition (EMT), resulting in hyperplasia of the gastrointestinal epithelium, fibrosis in the pancreas and liver, and increased proliferation of the pancreatic and hepatic bile ducts [2]. In mice, knockout of Dact2 alleviated cisplatin-induced nephrotoxicity. RNA sequencing revealed differences in gene expression related to cell proliferation, apoptosis, and the MAPK pathway between wild-type and Dact2 knockout mice. β-catenin was found to directly bind to and regulate the transcription of Igf1, which was involved in the alleviation of cisplatin-induced cytotoxicity [3].

In conclusion, Dact2 is an important regulator of key signaling pathways. Gene knockout models in zebrafish and mice have revealed its role in processes like EMT, tissue fibrosis, and drug-induced nephrotoxicity. Understanding Dact2's function can provide insights into the mechanisms of these biological processes and disease conditions, potentially guiding the development of new treatment strategies.