Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
6017826 | Experimental Neurology | 2014 | 10 Pages |
Abstract
These results demonstrate that the UPR is strongly activated after neonatal HI. Over-activation of autophagy significantly reduces this response, highlighting the relevance of the cross-talk between ER and the autophagy machinery in this important pathological condition. Furthermore, the presence of ribosome subunits in autophagosome-like structures suggests that increased ribosome turnover through autophagy (ribophagy) may represent an additional mechanism involved in the neuroprotective effect observed after autophagy over-activation.
Keywords
LC3ATF-6ATF-4XBP-1GRP783MAeIF2αIRE1MDCp70S6KRAPmTORhsp70NeuN3-methyladenineC/EBPC/EBP homologous proteinPKR-like ER kinaseinositol-requiring enzyme 1AutophagyEndoplasmic reticulum (ER) stressanalysis of varianceANOVACHOPX-box binding protein-1Rapamycinendoplasmic reticulumactivating transcription factor-4activating transcription factor-6Monodansylcadaverinemammalian target of rapamycinhypoxia–ischemiaCCAAT/enhancer-binding proteinheat shock protein 70neuron-specific nuclear proteinPERKPostnatal
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Authors
Silvia Carloni, Maria Cristina Albertini, Luca Galluzzi, Giuseppe Buonocore, Fabrizio Proietti, Walter Balduini,