Prkd1, also known as PKCμ, encodes a serine/threonine protein kinase that is involved in a variety of fundamental cellular functions [4]. It is associated with pathways like the KRas-NF-κB pathway in pancreatic cancer, where the PRKD1 gene promoter is a target for oncogenic KRas signaling [2]. Prkd1 is important for biological processes such as cell-cell adhesion regulation in endothelial cells via the PKCμ/PRKD1-p38 MAPK-α-catenin signaling pathway [3].

In a Prkd1 transgenic mouse model (Prkd1em1) with deletion of exon 2 causing loss of function, homozygous deletion of Prkd1 is associated with complex congenital heart diseases (CHDs) like atrioventricular septal defects, bicuspid aortic and pulmonary valves, and is lethal. Even in heterozygotes, cardiac differences occur [4]. In osteocytes, inhibition or genetic deletion of Prkd1 in mice slows plasma membrane disruption (PMD) repair rate and impairs post-wounding cell survival. In vivo, Prkd1 conditional knockout (CKO) mice show blunted anabolic responses to tibial loading [1].

In conclusion, Prkd1 plays a pivotal role in heart development, the repair of plasma membrane disruptions in osteocytes, and is associated with CHDs. The study of Prkd1 through gene knockout and conditional knockout mouse models provides important insights into its functions in these biological processes and disease conditions.