{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Zhang L"],"funding":["Austrian Science Fund FWF","Deutsche Forschungsgemeinschaft (German Research Foundation)"],"pagination":["1348"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12449474"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["8(1)"],"pubmed_abstract":["Ion transport within mitochondria influences their structure, energy production, and cell death regulation. TMBIM5, a conserved calcium/proton exchanger in the inner mitochondrial membrane, contributes to mitochondrial structure, ATP synthesis, and apoptosis regulation. The relationship of TMBIM5 with the mitochondrial calcium uniporter complex formed by MCU, MICU1-3, and EMRE remains undefined. We generated Tmbim5-deficient Drosophila that exhibit disrupted cristae architecture, premature mitochondrial permeability transition pore opening, reduced calcium uptake, and mitochondrial swelling - resulting in impaired mobility and shortened lifespan. Crossing these with flies lacking mitochondrial calcium uniporter complex proteins was generally detrimental, but partial MICU1 depletion amelior"],"journal":["Communications biology"],"pubmed_title":["Interaction of the mitochondrial calcium/proton exchanger TMBIM5 with MICU1."],"pmcid":["PMC12449474"],"funding_grant_id":["ME1922/17-1","10.55776/COE14."],"pubmed_authors":["Garg V","Bueno D","Graier WF","Methner A","Dietsche F","Bitar S","Rojas-Charry L","Zhang L","Gottschalk B","Kumari A"],"additional_accession":[]},"is_claimable":false,"name":"Interaction of the mitochondrial calcium/proton exchanger TMBIM5 with MICU1.","description":"Ion transport within mitochondria influences their structure, energy production, and cell death regulation. TMBIM5, a conserved calcium/proton exchanger in the inner mitochondrial membrane, contributes to mitochondrial structure, ATP synthesis, and apoptosis regulation. The relationship of TMBIM5 with the mitochondrial calcium uniporter complex formed by MCU, MICU1-3, and EMRE remains undefined. We generated Tmbim5-deficient Drosophila that exhibit disrupted cristae architecture, premature mitochondrial permeability transition pore opening, reduced calcium uptake, and mitochondrial swelling - resulting in impaired mobility and shortened lifespan. Crossing these with flies lacking mitochondrial calcium uniporter complex proteins was generally detrimental, but partial MICU1 depletion amelior","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Sep","modification":"2026-06-03T17:29:15.489Z","creation":"2026-04-29T03:13:26.771Z"},"accession":"S-EPMC12449474","cross_references":{"pubmed":["40973741"],"doi":["10.1038/s42003-025-08839-6"]}}