Authors show that the genetic ablation of hace1 in the YAC128 mouse model of HD accelerates motor deficits and exacerbates cognitive and psychiatric phenotypes in vivo.
HACE1 controls TNF-elicited cell fate decisions and exerts tumor suppressor and anti-inflammatory activities via a TNFR1-RIP3 kinase-necroptosis pathway.
Increased reactive oxygen species (ROS) production due to Hace1 loss leads to glutamine addiction as a mechanism to cope with increased ROS-induced oxidative stress.
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