{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Cheng L"],"funding":["Natural Science Foundation of Shandong Province","the Fundamental Research Funds of Chinese Academy of Medical Sciences","Shandong University Multidisciplinary Research and Innovation Team of Young Scholars","the National Natural Science Foundation of China"],"pagination":["135"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11971201"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["50(2)"],"pubmed_abstract":["The accumulation of amyloid β (Aβ) protein, derived from the amyloid precursor protein (APP), plays a pivotal role in the pathogenesis of Alzheimer's disease (AD) by inducing neuronal cell injury. This study investigated the specific functions of ubiquitin-specific protease 1-associated factor 1 (UAF1) in mediating the neurotoxic effects triggered on Aβ. To model AD-related neuronal injury in vitro and in vitro, SH-SY5Y cells exposed to Aβ<sub>25-35</sub> and APPswe/PS1dE9 (APP/PS1) transgenic mice were utilized. Compared with control mice, UAF1 levels were significantly elevated in the hippocampus of experimental mice. In vitro experiments showed that UAF1 knockdown reduced Aβ-induced apoptosis and enhanced cell viability. Furthermore, UAF1 knockdown markedly suppressed Aβ<sub>25-35</sub>"],"journal":["Neurochemical research"],"pubmed_title":["Targeting UAF1 Alleviate Neurotoxicity by Inhibiting APP/NLRP3 Axis-Mediated Pyroptosis and Apoptosis."],"pmcid":["PMC11971201"],"funding_grant_id":["81870848","2020QNQT019","2019-RC-HL-026","ZR2023MH340"],"pubmed_authors":["Yang H","Xiao Y","Li F","Xie Z","Cheng L","Zheng B","Tian D","Meng X","Bi J","Zhao X","Xu Y"],"additional_accession":[]},"is_claimable":false,"name":"Targeting UAF1 Alleviate Neurotoxicity by Inhibiting APP/NLRP3 Axis-Mediated Pyroptosis and Apoptosis.","description":"The accumulation of amyloid β (Aβ) protein, derived from the amyloid precursor protein (APP), plays a pivotal role in the pathogenesis of Alzheimer's disease (AD) by inducing neuronal cell injury. This study investigated the specific functions of ubiquitin-specific protease 1-associated factor 1 (UAF1) in mediating the neurotoxic effects triggered on Aβ. To model AD-related neuronal injury in vitro and in vitro, SH-SY5Y cells exposed to Aβ<sub>25-35</sub> and APPswe/PS1dE9 (APP/PS1) transgenic mice were utilized. Compared with control mice, UAF1 levels were significantly elevated in the hippocampus of experimental mice. In vitro experiments showed that UAF1 knockdown reduced Aβ-induced apoptosis and enhanced cell viability. Furthermore, UAF1 knockdown markedly suppressed Aβ<sub>25-35</sub>","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Apr","modification":"2025-07-03T03:04:32.272Z","creation":"2025-07-03T03:04:32.272Z"},"accession":"S-EPMC11971201","cross_references":{"pubmed":["40183841"],"doi":["10.1007/s11064-025-04379-x"]}}