{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Gordaliza-Alaguero I"],"funding":["Instituto de Salud Carlos III","Fundación BBVA","Centers of Excellence Severo Ochoa Award","“La Caixa” Foundation","Fundació Marató de TV3","FEDER -A Way of making Europe","ERDF Operational Program in Catalonia","European Union’s Horizon 2020 Research and Innovation Programme","European Regional Development Fund","CERCA Programe of the Generalitat de Catalunya"],"pagination":["957-978"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12013434"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["21(5)"],"pubmed_abstract":["MFN1 (mitofusin 1) and MFN2 are key players in mitochondrial fusion, endoplasmic reticulum (ER)-mitochondria juxtaposition, and macroautophagy/autophagy. However, the mechanisms by which these proteins participate in these processes are poorly understood. Here, we studied the interactomes of these two proteins by using CRISPR-Cas9 technology to insert an HA-tag at the C terminus of MFN1 and MFN2, and thus generating HeLa cell lines that endogenously expressed MFN1-HA or MFN2-HA. HA-affinity isolation followed by mass spectrometry identified potential interactors of MFN1 and MFN2. A substantial proportion of interactors were common for MFN1 and MFN2 and were regulated by nutrient deprivation. We validated novel ER and endosomal partners of MFN1 and/or MFN2 with a potential role in interorga"],"journal":["Autophagy"],"pubmed_title":["Endogenous interactomes of MFN1 and MFN2 provide novel insights into interorganelle communication and autophagy."],"pmcid":["PMC12013434"],"funding_grant_id":["PID2021-122909NB-I00","IU16–015983","20132330","LCF/PR/HR21/52410007","PID2022-137576OB-I00","945352"],"pubmed_authors":["Sanchez-Fernandez-de-Landa P","Ivanova S","Martinez-Vicente M","Martin-Malpartida P","Seco J","Palacin M","Arauz-Garofalo G","Radivojevikj D","Gordaliza-Alaguero I","Vilaseca M","Zorzano A","Macias MJ","Gay M","Villarreal L"],"additional_accession":[]},"is_claimable":false,"name":"Endogenous interactomes of MFN1 and MFN2 provide novel insights into interorganelle communication and autophagy.","description":"MFN1 (mitofusin 1) and MFN2 are key players in mitochondrial fusion, endoplasmic reticulum (ER)-mitochondria juxtaposition, and macroautophagy/autophagy. However, the mechanisms by which these proteins participate in these processes are poorly understood. Here, we studied the interactomes of these two proteins by using CRISPR-Cas9 technology to insert an HA-tag at the C terminus of MFN1 and MFN2, and thus generating HeLa cell lines that endogenously expressed MFN1-HA or MFN2-HA. HA-affinity isolation followed by mass spectrometry identified potential interactors of MFN1 and MFN2. A substantial proportion of interactors were common for MFN1 and MFN2 and were regulated by nutrient deprivation. We validated novel ER and endosomal partners of MFN1 and/or MFN2 with a potential role in interorga","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 May","modification":"2026-06-12T04:58:59.078Z","creation":"2026-06-12T03:08:19.802Z"},"accession":"S-EPMC12013434","cross_references":{"pubmed":["39675054"],"doi":["10.1080/15548627.2024.2440843"]}}