Cdk17, also known as PCTAIRE-2, belongs to the PCTAIRE subfamily of cyclin-dependent kinases (CDKs). Although the full-scope of its functions is still being explored, kinases in this family are generally involved in cell signaling pathways, which are fundamental for normal cellular function. Dysregulation of such kinases can lead to various pathological conditions, highlighting the importance of understanding Cdk17's role [2].

In the context of liver fibrosis, miR-199a-3p was found to alleviate thioacetamide-induced liver fibrosis in a mouse model by directly downregulating Cdk17. Depletion of Cdk17 alone in activated hepatic stellate cells (HSCs) suppressed their activation, function, proliferation, and viability, mirroring the effects of miR-199a mimic treatment. This indicates that Cdk17 plays a role in promoting the activation and function of HSCs, which are central drivers of liver fibrosis [1].

In glioma research, through bioinformatics analysis of gene expression profiles, Cdk17 was identified as one of the key genes, suggesting it may play important roles in glioma prognosis and treatment, though the exact mechanisms remain to be further explored [3].

In conclusion, Cdk17 appears to be involved in multiple biological processes and disease conditions. The findings from liver fibrosis and glioma studies suggest its potential as a therapeutic target. Model-based research, such as the mouse model in liver fibrosis, has been crucial in uncovering these functions, contributing to our understanding of its role in specific disease areas.