Calpain-2 nucleocytoplasmic trafficking is involved in preconditioning-induced neuronal ischemic tolerance

Poster del trabajo presentado en el 43rd Annual Meeting of the Spanish Society of Biochemistry & Molecular Biology, celebrado en Barcelona, del 19 al 22 de julio de 2021The activation or inhibition of specific signalling pathways mediated by subtoxic stimulus, called preconditioning (PC), is one of the most important endogenous mechanisms re- sponsible for increased brain tolerance against ischemia [1]. In patients, we confirmed that transient ischemic attack (TIA) prior to ischemic stroke represent a clinical equivalent of brain PC [2]. Furthermore, we described that ischemic PC (IPC) increases MDM2-p53 complex interaction, which prevents ischemia-induced p53 stabilization, leading to neuronal ischemic toleranc (IT) in both “in vitro” and “in vivo” stroke models [3]ISCIII: PI18/00103 - PI18/00285 - RD16/0019/0018 -FEDER European regional development fund - JCyL: IES007P17 - CLU201703 P.O.FEDER CyL1420 and EDU/556/201