Cdk13, a cyclin-dependent kinase, phosphorylates the C-terminal domain of RNA polymerase II, regulating transcription and co-transcriptional processes [3,5,7]. It is involved in nuclear RNA surveillance pathways [2], lipid metabolism-related gene transcription [4], and may phosphorylate translation machinery components [6]. It is also important for the proper expression of numerous genes [7].

Mutations in Cdk13 have been identified as a cause of syndromic intellectual disability, with characteristic craniofacial features, feeding difficulties in infancy, and structural heart or brain malformations [1]. Oncogenic Cdk13 mutations impede nuclear RNA surveillance, accelerating melanoma in zebrafish [2]. In triple-negative breast cancer, targeting Cdk13 (along with Cdk12) can trigger intronic polyadenylation site cleavage, suppressing DNA damage response proteins [3]. In prostate cancer, Cdk13 promotes lipid deposition and cancer progression via a Cdk13/NSUN5/ACC1 pathway [4]. In colorectal cancer, Cdk13 phosphorylates translation machinery components, promoting protein synthesis and cell proliferation [6].

In conclusion, Cdk13 is crucial for gene transcription regulation, RNA surveillance, and lipid metabolism-related gene expression. Studies on Cdk13-related mutations in various genetic models, such as zebrafish in melanoma research [2], have revealed its significant roles in neurodevelopmental disorders and multiple cancers, highlighting its potential as a therapeutic target in these disease areas.