{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["18(4)"],"submitter":["Bartlett R"],"funding":["FightMND","R. Howard Webster Foundation","Motor Neurone Disease Research Institute of Australia","ALS Society of Canada","The University of Wollongong","Canadian Consortium for Neurodegeneration in Aging","Brain Canada","National Health and Medical Research Council"],"pubmed_abstract":["Mutant superoxide dismutase 1 (SOD1) can be constitutively released from motor neurons and transmitted to naïve motor neurons to promote the progression of amyotrophic lateral sclerosis (ALS). However, the biological impacts of this process and the precise mechanisms of SOD1 release remain to be fully resolved. Using biochemical and fluorescent techniques, this study aimed to determine if P2X7 receptor activation could induce mutant SOD1 release from motor neurons and whether this released SOD1 could be transmitted to motor neurons or microglia to mediate effects associated with neurodegeneration in ALS. Aggregated SOD1<sup>G93A</sup>, released from murine NSC-34 motor neurons transiently transfected with SOD1<sup>G93A</sup>, could be transmitted to naïve NSC-34 cells and murine EOC13 micr"],"journal":["Purinergic signalling"],"pagination":["451-467"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9832181"],"repository":["biostudies-literature"],"pubmed_title":["P2X7 receptor activation mediates superoxide dismutase 1 (SOD1) release from murine NSC-34 motor neurons."],"pmcid":["PMC9832181"],"pubmed_authors":["Cashman NR","Sluyter R","Ly D","Yerbury JJ","Bartlett R"],"additional_accession":[]},"is_claimable":false,"name":"P2X7 receptor activation mediates superoxide dismutase 1 (SOD1) release from murine NSC-34 motor neurons.","description":"Mutant superoxide dismutase 1 (SOD1) can be constitutively released from motor neurons and transmitted to naïve motor neurons to promote the progression of amyotrophic lateral sclerosis (ALS). However, the biological impacts of this process and the precise mechanisms of SOD1 release remain to be fully resolved. Using biochemical and fluorescent techniques, this study aimed to determine if P2X7 receptor activation could induce mutant SOD1 release from motor neurons and whether this released SOD1 could be transmitted to motor neurons or microglia to mediate effects associated with neurodegeneration in ALS. Aggregated SOD1<sup>G93A</sup>, released from murine NSC-34 motor neurons transiently transfected with SOD1<sup>G93A</sup>, could be transmitted to naïve NSC-34 cells and murine EOC13 micr","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Dec","modification":"2025-05-29T16:17:38.838Z","creation":"2025-04-19T23:05:43.882Z"},"accession":"S-EPMC9832181","cross_references":{"pubmed":["35478453"],"doi":["10.1007/s11302-022-09863-5"]}}