Dusp10, also known as MAP kinase phosphatase 5 (MKP5), is a member of the dual-specificity phosphatase family. It negatively regulates the activation of mitogen-activated protein kinases (MAPKs), including p38 MAPK, c-Jun N-terminal kinase (JNK), and in some cases, extracellular signal-regulated kinase (ERK). This regulation impacts various cellular processes such as cytokine secretion, proliferation, survival, and apoptosis, thus being of great biological importance. Genetic models, like gene knockout mouse models, are valuable for studying Dusp10's functions [2].

In ischemic stroke, Dusp10 overexpression improved neuronal survival and reduced apoptosis by inhibiting the p38/JNK signaling pathway, while knockdown exacerbated infarct volume and neuronal damage [1]. In colorectal cancer, Dusp10 knockout mice had increased intestinal epithelial cell proliferation and developed more colon tumours, indicating that Dusp10 acts as a suppressor for CRC [3]. In non-small cell lung cancer, overexpression of Dusp10 increased cellular growth and migration, and was associated with increased expression of tumor-promoting cytokines, suggesting its oncogenic role [4].

In conclusion, Dusp10 is a key regulator of MAPK-related pathways and plays diverse roles in different diseases. Gene knockout mouse models have been crucial in revealing its functions in ischemic stroke, colorectal cancer, and non-small cell lung cancer, among others. Understanding Dusp10's functions provides insights into disease mechanisms and potential therapeutic targets.