{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Deepa SS"],"funding":["BLRD VA","NIA NIH HHS","Oklahoma Center for Adult Stem Cell Research","NCI NIH HHS","American Federation for Aging Research","National Institutes of Health","Department of Veterans Affairs","NIGMS NIH HHS"],"pagination":["102854"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC10990772"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["119"],"pubmed_abstract":["The necroptotic effector molecule MLKL accumulates in neurons over the lifespan of mice, and its downregulation has the potential to improve cognition through neuroinflammation, and changes in the abundance of synaptic proteins and enzymes in the central nervous system. Notwithstanding, direct evidence of cell-autonomous effects of MLKL expression on neuronal physiology and metabolism are lacking. Here, we tested whether the overexpression of MLKL in the absence of cell death in the neuronal cell line Neuro-2a recapitulates some of the hallmarks of aging at the cellular level. Using genetically-encoded fluorescent biosensors, we monitored the cytosolic and mitochondrial Ca<sup>2+</sup> levels, along with the cytosolic concentrations of several metabolites involved in energy metabolism (lac"],"journal":["Cell calcium"],"pubmed_title":["MLKL overexpression leads to Ca&lt;sup&gt;2+&lt;/sup&gt; and metabolic dyshomeostasis in a neuronal cell model."],"pmcid":["PMC10990772"],"funding_grant_id":["P30 AG050911","P20 GM125528","R03 CA262044","R01 AG059718","IK6 BX005238","I01 BX004538"],"pubmed_authors":["Richardson A","Thadathil N","Mohammed S","Rose H","Diaz-Garcia CM","Pham S","Kinter MT","Deepa SS","Corral J"],"additional_accession":[]},"is_claimable":false,"name":"MLKL overexpression leads to Ca&lt;sup&gt;2+&lt;/sup&gt; and metabolic dyshomeostasis in a neuronal cell model.","description":"The necroptotic effector molecule MLKL accumulates in neurons over the lifespan of mice, and its downregulation has the potential to improve cognition through neuroinflammation, and changes in the abundance of synaptic proteins and enzymes in the central nervous system. Notwithstanding, direct evidence of cell-autonomous effects of MLKL expression on neuronal physiology and metabolism are lacking. Here, we tested whether the overexpression of MLKL in the absence of cell death in the neuronal cell line Neuro-2a recapitulates some of the hallmarks of aging at the cellular level. Using genetically-encoded fluorescent biosensors, we monitored the cytosolic and mitochondrial Ca<sup>2+</sup> levels, along with the cytosolic concentrations of several metabolites involved in energy metabolism (lac","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 May","modification":"2026-06-02T20:58:43.565Z","creation":"2025-07-13T03:04:44.481Z"},"accession":"S-EPMC10990772","cross_references":{"pubmed":["38430790"],"doi":["10.1016/j.ceca.2024.102854"]}}