A role for caspase-8 and TRAIL-R2/DR5 in ER-stress induced apoptosis

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dc.contributor.author	Muñoz Pinedo, Cristina
dc.contributor.author	López Rivas, Abelardo
dc.date	2017-11-27T15:13:58Z
dc.date	2018-04-06T22:01:23Z
dc.date	2017-10-06
dc.identifier.citation	1476-5403
dc.identifier.uri	http://hdl.handle.net/2445/118182
dc.format	5 p.
dc.format	5 p.
dc.format	application/pdf
dc.language.iso	eng
dc.publisher	Nature Publishing Group
dc.relation	Reproducció del document publicat a: http://dx.doi.org/10.1038/cdd.2017.155
dc.relation	Cell Death & Differentiation, 2017, num. 1 October
dc.relation	http://dx.doi.org/10.1038/cdd.2017.155
dc.rights	(c) Cell Death & Differentiation, 2017
dc.rights	info:eu-repo/semantics/openAccess
dc.subject	Proteïnes
dc.subject	Apoptosi
dc.subject	Proteins
dc.subject	Apoptosis
dc.title	A role for caspase-8 and TRAIL-R2/DR5 in ER-stress induced apoptosis
dc.type	info:eu-repo/semantics/other
dc.type	info:eu-repo/semantics/acceptedVersion
dc.description.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.

Cano-González, Ana; Mauro-Lizcano, Marta; Iglesias i Serret, Daniel; Gil i Santano, Joan; López Rivas, Abelardo

Püschel, Franziska; Muñoz Pinedo, Cristina

Pfeiffer, S.; Anilkumar, U.; Chen, G.; Ramírez Peinado, Silvia; Galindo Moreno, Javier; Muñoz Pinedo, Cristina; Prehn, J. M. H.

Muñoz Pinedo, Cristina; Martin, S. J.

Galindo Moreno, Javier; Iurlaro, Raffaella; Mjiyad, Nadia El; Díez Pérez, J.; Gabaldón, T.; Muñoz Pinedo, Cristina

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