Abstract:
|
Glab and colleagues examine in a recent paper apoptosis induced by some driverss of
endoplasmic reticulum (ER) stress. They conclude that in contrast to a previously published
report2
, DR5/TRAIL-R2 and caspase-8 are universally dispensable in ER stress-induced
apoptosis. We argue here that their own data and other published reports indicate that in
many models, DR5 and/or caspase-8 are essential players in apoptosis mediated by the
unfolded protein response (UPR), upon chronic ER stress. |