{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Di Benedetto G"],"funding":["PRIN from the Italian Ministry of Research."],"pagination":["11625"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9569968"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["23(19)"],"pubmed_abstract":["TRAIL, a member of TNF superfamily, is a potent inducer of neuronal death. Neurotoxic effects of TRAIL appear mediated by its death receptor TRAIL-R2/DR5. To assess the role of TRAIL/TRAIL-R2 pathway in AD-related neurodegeneration, we studied the impact of the treatment with amyloid-β (Aβ) upon cell viability and inflammation in TRAIL-R-deficient mice (TRAIL-R<sup>-/-</sup>). Here, we demonstrate that the lack of TRAIL-R2 protects from death cultured TRAIL-R<sup>-/-</sup> mouse embryonic hippocampal cells after treatment with either Aβ1-42 or TRAIL. Consistently, stereotaxic injection of Aβ1-42 resulted in blunted caspase activation, as well as in reduction of JNK phosphorylation and increased AKT phosphorylation in TRAIL-R<sup>-/-</sup> mice. Moreover, the lack of TRAIL-R2 was associated"],"journal":["International journal of molecular sciences"],"pubmed_title":["TRAIL-R Deficient Mice Are Protected from Neurotoxic Effects of Amyloid-β."],"pmcid":["PMC9569968"],"funding_grant_id":["2017YH3SXK"],"pubmed_authors":["Di Mauro R","Caltabiano R","Bellanca CM","Burgaletto C","Cantarella G","Bernardini R","Munafo A","Di Benedetto G","Serapide MF"],"additional_accession":[]},"is_claimable":false,"name":"TRAIL-R Deficient Mice Are Protected from Neurotoxic Effects of Amyloid-β.","description":"TRAIL, a member of TNF superfamily, is a potent inducer of neuronal death. Neurotoxic effects of TRAIL appear mediated by its death receptor TRAIL-R2/DR5. To assess the role of TRAIL/TRAIL-R2 pathway in AD-related neurodegeneration, we studied the impact of the treatment with amyloid-β (Aβ) upon cell viability and inflammation in TRAIL-R-deficient mice (TRAIL-R<sup>-/-</sup>). Here, we demonstrate that the lack of TRAIL-R2 protects from death cultured TRAIL-R<sup>-/-</sup> mouse embryonic hippocampal cells after treatment with either Aβ1-42 or TRAIL. Consistently, stereotaxic injection of Aβ1-42 resulted in blunted caspase activation, as well as in reduction of JNK phosphorylation and increased AKT phosphorylation in TRAIL-R<sup>-/-</sup> mice. Moreover, the lack of TRAIL-R2 was associated","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Oct","modification":"2025-04-18T19:32:48.981Z","creation":"2024-11-06T04:34:51.993Z"},"accession":"S-EPMC9569968","cross_references":{"pubmed":["36232931"],"doi":["10.3390/ijms231911625"]}}