{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["4(3)"],"submitter":["Xiao T"],"funding":["Howard Hughes Medical Institute","NIA NIH HHS","NIGMS NIH HHS"],"pubmed_abstract":["Deficiencies in mitochondrial import cause the toxic accumulation of non-imported mitochondrial precursor proteins. Numerous fates for non-imported mitochondrial precursors have been identified in budding yeast, including proteasomal destruction, deposition into protein aggregates, and mistargeting to other organelles. Amongst organelles, the ER has emerged as a key destination for a subset of non-imported mitochondrial proteins. However, how ER targeting of various types of mitochondrial proteins is achieved remains incompletely understood. Here, we show that the ER delivery of endogenous mitochondrial transmembrane proteins, especially those belonging to the SLC25A mitochondrial carrier family, is dependent on the guided entry of tail-anchored proteins (GET) complex. Without a functional"],"journal":["Life science alliance"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC7898604"],"repository":["biostudies-literature"],"pubmed_title":["ER targeting of non-imported mitochondrial carrier proteins is dependent on the GET pathway."],"pmcid":["PMC7898604"],"funding_grant_id":["R35 GM119694","R01 AG061376"],"pubmed_authors":["Shakya VP","Hughes AL","Xiao T"],"additional_accession":[]},"is_claimable":false,"name":"ER targeting of non-imported mitochondrial carrier proteins is dependent on the GET pathway.","description":"Deficiencies in mitochondrial import cause the toxic accumulation of non-imported mitochondrial precursor proteins. Numerous fates for non-imported mitochondrial precursors have been identified in budding yeast, including proteasomal destruction, deposition into protein aggregates, and mistargeting to other organelles. Amongst organelles, the ER has emerged as a key destination for a subset of non-imported mitochondrial proteins. However, how ER targeting of various types of mitochondrial proteins is achieved remains incompletely understood. Here, we show that the ER delivery of endogenous mitochondrial transmembrane proteins, especially those belonging to the SLC25A mitochondrial carrier family, is dependent on the guided entry of tail-anchored proteins (GET) complex. Without a functional","dates":{"release":"2021-01-01T00:00:00Z","publication":"2021 Mar","modification":"2025-04-21T23:37:59.102Z","creation":"2025-04-05T19:12:51.934Z"},"accession":"S-EPMC7898604","cross_references":{"pubmed":["33479049"],"doi":["10.26508/lsa.202000918"]}}