Our ongoing analysis of embryos with mutated chromatin-remodeling enzymes has piqued our interest in the protein RIPK3, which is best known as a key executor of the programmed necrosis (necroptosis) cell death pathway. We recently reported that embryonic vessels with elevated endothelial RIPK3 expression are prone to rupture (Colijn, Gao, Ingram et al, 2019). However, this vascular fragility appears to be unrelated to necroptosis, which implies that excessive RIPK3 can play other detrimental roles in endothelial cells. Several ongoing projects in the lab are focused on physiological and pathological roles for endothelial RIPK3 and its impact on vascular development and maintenance.
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