Molecular Function of Midnolin and Its Relevance to Parkinson's Disease.

Midnolin () was originally discovered as a gene expressed specifically in the mouse midbrain at the embryonic developmental stage; MIDN was localized in the nucleus/nucleolus. Although the pathophysiological roles of MIDN remained largely unknown for many years after its discovery, its molecular functions and relevance to diseases have gradually become clearer. In PC12 cells, a rat neuronal model cell line, liquidity factors that are necessary for neurite outgrowth are reported to induce gene expression. In addition, MIDN is required for E3 ubiquitin-protein ligase parkin expression, suggesting that MIDN is important for the development and maintenance of neuronal functions. Notably, it was recently reported that MIDN plays fundamental roles in the ubiquitin-independent proteasomal degradation of various nuclear proteins and transcription factors. Regarding the relationship between MIDN and diseases, copy number loss of is associated with Parkinson's disease, suggesting that is a genetic risk factor for this disease. In addition, MIDN is relevant to many types of malignant cancer, including B-cell lymphoma and liver cancer. Thus, MIDN is an essential molecule for the maintenance of homeostasis, and its functional disorder triggers multiple diseases depending on the affected tissues/organs. therefore shows promise as a potential therapeutic target and prognostic biomarker.