000070296 001__ 70296
000070296 005__ 20200117221639.0
000070296 0247_ $$2doi$$a10.1038/s41419-018-0408-1
000070296 0248_ $$2sideral$$a105320
000070296 037__ $$aART-2018-105320
000070296 041__ $$aeng
000070296 100__ $$aElena-Real, C.A.
000070296 245__ $$aCytochrome c speeds up caspase cascade activation by blocking 14-3-3¿-dependent Apaf-1 inhibition article
000070296 260__ $$c2018
000070296 5060_ $$aAccess copy available to the general public$$fUnrestricted
000070296 5203_ $$aApoptosis is a highly regulated form of programmed cell death, essential to the development and homeostasis of multicellular organisms. Cytochrome c is a central figure in the activation of the apoptotic intrinsic pathway, thereby activating the caspase cascade through its interaction with Apaf-1. Our recent studies have revealed 14-3-3€ (a direct inhibitor of Apaf-1) as a cytosolic cytochrome c target. Here we explore the cytochrome c / 14-3-3€ interaction and show the ability of cytochrome c to block 14-3-3€-mediated Apaf-1 inhibition, thereby unveiling a novel function for cytochrome c as an indirect activator of caspase-9/3. We have used calorimetry, NMR spectroscopy, site mutagenesis and computational calculations to provide an insight into the structural features of the cytochrome c / 14-3-3€ complex. Overall, these findings suggest an additional cytochrome c-mediated mechanism to modulate apoptosome formation, shedding light onto the rigorous apoptotic regulation network.
000070296 536__ $$9info:eu-repo/grantAgreement/ES/MINECO/BFU2013-47064P-BMC$$9info:eu-repo/grantAgreement/ES/MINECO/BFU2015-71017-P-BMC$$9info:eu-repo/grantAgreement/ES/MINECO/SAF2015-64383-P
000070296 540__ $$9info:eu-repo/semantics/openAccess$$aby$$uhttp://creativecommons.org/licenses/by/3.0/es/
000070296 590__ $$a5.959$$b2018
000070296 591__ $$aCELL BIOLOGY$$b38 / 191 = 0.199$$c2018$$dQ1$$eT1
000070296 592__ $$a2.31$$b2018
000070296 593__ $$aCancer Research$$c2018$$dQ1
000070296 593__ $$aCell Biology$$c2018$$dQ1
000070296 593__ $$aMedicine (miscellaneous)$$c2018$$dQ1
000070296 593__ $$aImmunology$$c2018$$dQ1
000070296 593__ $$aCellular and Molecular Neuroscience$$c2018$$dQ1
000070296 655_4 $$ainfo:eu-repo/semantics/article$$vinfo:eu-repo/semantics/publishedVersion
000070296 700__ $$aDíaz-Quintana, A.
000070296 700__ $$aGonzález-Arzola, K.
000070296 700__ $$0(orcid)0000-0001-5702-4538$$aVelázquez-Campoy, A.$$uUniversidad de Zaragoza
000070296 700__ $$aOrzáez, M.
000070296 700__ $$aLópez-Rivas, A.
000070296 700__ $$aGil-Caballero, S.
000070296 700__ $$aDe La Rosa, M.Á.
000070296 700__ $$aDíaz-Moreno, I.
000070296 7102_ $$11002$$2060$$aUniversidad de Zaragoza$$bDpto. Bioq.Biolog.Mol. Celular$$cÁrea Bioquímica y Biolog.Mole.
000070296 773__ $$g9, 3 (2018), 365 [12 pp]$$pCell death dis.$$tCell death & disease$$x2041-4889
000070296 8564_ $$s1460088$$uhttps://zaguan.unizar.es/record/70296/files/texto_completo.pdf$$yVersión publicada
000070296 8564_ $$s107903$$uhttps://zaguan.unizar.es/record/70296/files/texto_completo.jpg?subformat=icon$$xicon$$yVersión publicada
000070296 909CO $$ooai:zaguan.unizar.es:70296$$particulos$$pdriver
000070296 951__ $$a2020-01-17-22:03:19
000070296 980__ $$aARTICLE