Abstract
In this issue of PLOS Biology, Zhang and colleagues unveil a complex midgestational death during embryogenesis of mice harboring caspase-8 cleavage-resistant receptor-interacting protein (RIP) kinase (RIPK)1. Tumor necrosis factor (TNF) receptor (TNFR)1-dependent signaling drives cell death through a novel pathway requiring synergism between apoptotic and pyroptotic caspases.
Highlights
In this issue of PLOS Biology, Zhang and colleagues unveil a complex midgestational death during embryogenesis of mice harboring caspase-8 cleavage-resistant receptor-interacting protein (RIP) kinase (RIPK)1
The results presented indicate that theAcUlea:vaAgneaobfbRreIvPiKat1iobnylicsathspaasbsee-e8nrceosmtrpailnesdRfoIrPthKo1s-emuseeddiathterdouagchtiovuat-thetext:Plea tion of both apoptotic and pyroptotic caspases
Mice, even though the second allele remains wild type [5,6,7]. While it remains to be resolved whether noncleavable RIPK1 mediates its gain-of-function effects because of increased stability or because of some novel structural feature conferring increased activity, the Zhang and colleagues study provides new insights into the mechanisms through which RIPK1 determines cell fate in the course of development and regulates inflammatory homeostasis throughout life
Summary
In this issue of PLOS Biology, Zhang and colleagues unveil a complex midgestational death during embryogenesis of mice harboring caspase-8 cleavage-resistant receptor-interacting protein (RIP) kinase (RIPK)1. Tumor necrosis factor (TNF) receptor (TNFR)1-dependent signaling drives cell death through a novel pathway requiring synergism between apoptotic and pyroptotic caspases.
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
