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Journal Article
DGKE disruption ditches complement and drives p38 signaling.
Blood 2015 Februrary 6
In this issue of Blood , Bruneau et al provide evidence that disruption of diacylglycerol kinase ε isoform (DGKε) does not upregulate complement activation, but rather induces endothelial damage via the activation of p38 mitogen–activated protein kinase (MAPK). These in vitro findings may support a new pathophysiologic mechanism for atypical hemolytic uremic syndrome (aHUS) in a subset of patients with DGKE gene mutations.
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