Cdk5r1, also known as cyclin-dependent kinase 5 regulatory subunit 1, encodes for p35, the main activator of Cyclin-dependent kinase 5 (CDK5). The active p35/CDK5 complex is involved in numerous aspects of brain development and function, and is associated with pathways like notch signaling [1,6]. It plays a crucial role in central nervous system development and neuronal migration [2].

In hepatocellular carcinoma (HCC), high Cdk5r1 expression is linked to adverse tumor status, new tumor events, clinical stage, topography, and worse survival outcomes, and can independently predict poor overall survival, disease-free interval, and progression-free interval [1]. In Schwann cells after sciatic nerve injury, overexpression of Cdk5r1 promotes cell proliferation, migration, and production of neurotrophic factors, and aids in nerve injury recovery through the CDK5/BDNF/TrkB pathway [2]. In Ewing's sarcoma cells, miR-152 suppresses cell proliferation by targeting Cdk5r1, and in multiple cancers including colorectal and breast malignancies, elevated Cdk5r1 expression is associated with poor prognosis, proliferation, and drug resistance [4,5]. In Alzheimer's disease, its down-regulation is related to specific subtypes and immune cell infiltration changes [3].

In conclusion, Cdk5r1 is essential for central nervous system development and neuronal migration. Studies, including those on various disease models, have shown its significance in cancer prognosis, peripheral nerve injury recovery, and neurodegenerative diseases. Understanding Cdk5r1 can provide insights into disease mechanisms and potential therapeutic targets.