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26%; Fig. 5F). To investigate putative signals acting downstream of SGK1 that may contribute to the vascular remodeling defects and the increase in endothelial cell death in Sgk1 null embryos, expression analyses were performed on signaling components of the Notch cascade, a critical pathway involved in angiogenesis (Adams, 2003; Liu et al., 2003). Although no significant differences were observed for the Notch receptors, Notch1 (P = 0.47) and Notch4 (P = 0.29), and the Notch ligand, Dll4 (P = 0.26), quantitative RT-PCR on cDNA of E9.0�CE9.5 embryos showed significant decrease of the Notch signaling ligand Jag1 (40%; P = 0.02) and the Epigenetic inhibitors Notch target gene Hey1 (60%; P = 0.019) in Sgk1 null embryos (Fig. 6A). Furthermore, consistent with the embryonic results, a significant reduction of the Notch signaling pathway was evident in Sgk1 null yolk sacs, considering that the expression levels of Jag1 (70%; P = 0.05) and the Notch target genes Hey1 (97%; P = 0.01) and Hey2 (98%; P = 0.04) were dramatically reduced PF-6463922 compared with the controls (Fig. 6B). Moreover, the expression levels of the Notch receptors Notch1 and Notch4 and the Notch ligand Dll4 remained unperturbed in Sgk1 null yolk sacs. To further verify whether the decreased Notch signaling observed in Sgk1 null embryos was confined to endothelial cells, primary cardiac endothelial cells (pCECs) from hearts of adult wild-type (+/+) and Sgk1 heterozygous (+/?) mice were isolated with a magnetic bead system using CD105 and Isolectin-��4 antibodies (Marelli-Berg et al., 2000; see the Experimental Procedures section). Quantitative RT-PCR studies Cefaloridine on cDNA of wild-type and Sgk1 heterozygous cells demonstrated significantly (P