Pkn1, or Protein kinase N1, is a serine/threonine kinase. It is involved in multiple biological processes, such as controlling Glut4 translocation and glucose transport, regulating synaptic maturation, and influencing cell aggregation and spheroid formation. It is also associated with pathways like AKT/GSK3β signaling. Pkn1 is important in adipocyte differentiation, glucose metabolism, and neural development, and its study via gene knockout models helps understand its functions [1,2,6].

In Pkn1 knockout mouse models, several effects have been observed. In the hippocampus, Pkn1 knockout led to elevated phospho-AKT and NeuroD2 levels, enhancing GluA1 expression [2]. In an in vitro model of cerebellar hypoxic-ischemic encephalopathy, Pkn1 -/- cerebellar granule cells showed higher AKT phosphorylation, reduced caspase-3 activation, and improved survival [4]. In the retina, Pkn1 knockout increased NeuroD2 levels and amacrine cell amount, while reducing SMI-32+ α-RGC [5]. Also, Pkn1[T778A] (kinase-deficient) mouse embryonic fibroblasts had delayed aggregate formation and abnormal spheroid compaction [6].

In summary, Pkn1 plays crucial roles in glucose metabolism, neural development, and cell-cell interactions. Studies using Pkn1 knockout mouse models have provided insights into its functions in diseases related to metabolism, neurodegeneration, and cancer. For example, in endometrial cancer, higher Pkn1 expression may be associated with poor prognosis [3]. These findings suggest Pkn1 could be a potential target for therapeutic interventions in relevant disease areas.