{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["13(1)"],"submitter":["Wang P"],"funding":["National Institutes of Health"],"pubmed_abstract":["<h4>Background</h4>Microtubule-binding protein tau is a misfolding-prone protein associated with tauopathies. As tau undergoes cell-to-cell transmission, extracellular tau aggregates convert astrocytes into a pro-inflammatory state via integrin activation, causing them to release unknown neurotoxic factors.<h4>Results</h4>Here, we combine transcriptomics with isotope labeling-based quantitative mass spectrometry analysis of mouse primary astrocyte secretome to establish PI3K-AKT as a critical differentiator between pathogenic and physiological integrin activation; simultaneous activation of PI3K-AKT and focal adhesion kinase (FAK) in tau fibril-treated astrocytes changes the output of integrin signaling, causing pro-inflammatory gene upregulation, trans-Golgi network restructuring, and alt"],"journal":["Cell & bioscience"],"pagination":["179"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC10536728"],"repository":["biostudies-literature"],"pubmed_title":["PI3K-AKT activation resculpts integrin signaling to drive filamentous tau-induced proinflammatory astrogliosis."],"pmcid":["PMC10536728"],"pubmed_authors":["Wang P","Anderson DE","Ye Y"],"additional_accession":[]},"is_claimable":false,"name":"PI3K-AKT activation resculpts integrin signaling to drive filamentous tau-induced proinflammatory astrogliosis.","description":"<h4>Background</h4>Microtubule-binding protein tau is a misfolding-prone protein associated with tauopathies. As tau undergoes cell-to-cell transmission, extracellular tau aggregates convert astrocytes into a pro-inflammatory state via integrin activation, causing them to release unknown neurotoxic factors.<h4>Results</h4>Here, we combine transcriptomics with isotope labeling-based quantitative mass spectrometry analysis of mouse primary astrocyte secretome to establish PI3K-AKT as a critical differentiator between pathogenic and physiological integrin activation; simultaneous activation of PI3K-AKT and focal adhesion kinase (FAK) in tau fibril-treated astrocytes changes the output of integrin signaling, causing pro-inflammatory gene upregulation, trans-Golgi network restructuring, and alt","dates":{"release":"2023-01-01T00:00:00Z","publication":"2023 Sep","modification":"2025-04-05T11:20:16.294Z","creation":"2025-02-19T03:36:45.888Z"},"accession":"S-EPMC10536728","cross_references":{"pubmed":["37759245"],"doi":["10.1186/s13578-023-01128-x"]}}