{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Russo MN"],"funding":["NIA NIH HHS","U.S. Department of Defense","NCI NIH HHS","NINDS NIH HHS","NIH HHS","Uncle Kory Foundation"],"pagination":["e70158"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12456098"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["14(9)"],"pubmed_abstract":["Glioblastoma (GBM), the most aggressive primary brain tumour in adults, presents significant challenges due to its universal recurrence and limited survival rates. A key driver of GBM progression is the subpopulation of brain tumour-initiating cells (BTICs), which contribute to therapy resistance and interact with the tumour microenvironment, particularly the cellular components in the subventricular zone (SVZ). Extracellular vesicles (EVs) are critical mediators of intercellular communication, carrying bioactive molecules, such as proteins and RNAs, that can modulate the behaviour of recipient cells. This study investigates the role of EVs in GBM's communication with non-cancer cells. We utilised the proximity-labelling system TurboID to achieve global and unbiased labelling of proteins w"],"journal":["Journal of extracellular vesicles"],"pubmed_title":["TurboID-Mediated Profiling of Glioblastoma-Derived Extracellular Vesicle Cargo Proteins."],"pmcid":["PMC12456098"],"funding_grant_id":["R01CA195503","K01NS110930","S10OD018034","5R01NS127187","R01AG067151-01A1","W81XWH-21-1-0182","RF1NS129032-01","S10OD019967","S10OD02365101A1","R01CA183827","R21NS128212-01A1"],"pubmed_authors":["Lam TT","Belzil VV","Zarco N","Wang W","Russo MN","Guerrero-Cazares H","Ulloa-Navas MJ","Norton ES","Quinones-Hinojosa A"],"additional_accession":[]},"is_claimable":false,"name":"TurboID-Mediated Profiling of Glioblastoma-Derived Extracellular Vesicle Cargo Proteins.","description":"Glioblastoma (GBM), the most aggressive primary brain tumour in adults, presents significant challenges due to its universal recurrence and limited survival rates. A key driver of GBM progression is the subpopulation of brain tumour-initiating cells (BTICs), which contribute to therapy resistance and interact with the tumour microenvironment, particularly the cellular components in the subventricular zone (SVZ). Extracellular vesicles (EVs) are critical mediators of intercellular communication, carrying bioactive molecules, such as proteins and RNAs, that can modulate the behaviour of recipient cells. This study investigates the role of EVs in GBM's communication with non-cancer cells. We utilised the proximity-labelling system TurboID to achieve global and unbiased labelling of proteins w","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Sep","modification":"2026-06-03T19:06:31.189Z","creation":"2026-04-30T03:12:06.979Z"},"accession":"S-EPMC12456098","cross_references":{"pubmed":["40985879"],"doi":["10.1002/jev2.70158"]}}