Since we observed impaired vessel formation in Prkcd and Prkce deficient embryos and allantois, we next performed a more detailed histological analysis to obtain further information regarding blood vessel structure. Via electron microscopy, wild type embryo sections showed that endothelial cells were properly interconnected and physically interacting with surrounding mural mesenchymal cells. In contrast, Prkcd and Prkce double deficient sections showed disassembled endothelial tubes with barely detectable endothelial-specific cell-cell adhesion molecules, i.e adherens junctions, as well as decreased contact with surrounding mural mesenchymal cells. Extracellular matrix-cell adhesion molecules were however detected at hemidesmosomes in both wild type and PRKCD and PRKCE double deficient embryo sections. In Isavuconazole addition, while apparently normal in wild type sections, histochemical analyses showed a small dorsal aorta in double deficient embryo sections, which was also suggested by our findings via CD31. Moreover, immunofluorescent detection of the VE-cadherin, an endothelial marker expressed at endothelial adherens junctions, appeared expressed at lower levels in the absence of PRKCD and PRKCE. Taken together, these data suggest that PRKCD and PRKCE are necessary for proper assembly and development of the vasculature, and for Testosterone undecanoate expression of CDH5 at the endothelial cell membrane. We recently showed that PRKCD and PRKCE display similar expression patterns in the mouse embryo during midgestation. Such similarity lead us to hypothesize that PRKCD and PRKCE could have redundant function in vivo that would explain the viability of both Prkcd and Prkce single deficient mice. For this reason, a mouse line containing null mutations for both Prkcd and Prkce was generated. Given the strong expression of these isoforms within the nervous system, finding an obvious phenotype within this domain would not have come as a surprise. However, we found that Prkcd and Prkce double deficiency caused lethality in mouse at E9.5, a stage at which the nervous system has not started to develop yet. The main observed phenotypes were growth retardation and swollen pericardium, which suggested impaired vascular development at this stage and a potential contributor to embryonic lethality.