Prkd1, also known as PKCμ, encodes a serine/threonine protein kinase. It is involved in multiple fundamental cellular functions and is associated with pathways like the KRas-NF-κB pathway in pancreatic cancer [2]. Prkd1 is crucial for normal development and disease processes in various tissues.

In mouse models, homozygous deletion of Prkd1 in a transgenic mouse model (Prkd1em1) led to complex congenital heart diseases (CHDs) such as atrioventricular septal defects and bicuspid aortic and pulmonary valves, and was lethal. Even heterozygotes showed cardiac differences, indicating its role in cardiogenesis [3]. In osteocytes, inhibition or genetic deletion of Prkd1 using an osteocyte-targeted (Dmp1-Cre) conditional knockout (CKO) mouse model slowed plasma membrane disruption (PMD) repair rate and impaired post-wounding cell survival, affecting in vivo bone anabolic responses to loading [1].

In conclusion, Prkd1 is essential for normal cardiac development and the repair of plasma membrane disruptions in osteocytes. The study of Prkd1 using gene knockout and conditional knockout mouse models has provided insights into its role in CHDs and bone-related biological processes, contributing to our understanding of the underlying mechanisms of these diseases.