{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nThe mitochondrial adenine nucleotide translocator 1 (ANT1), encoded by SLC25A4, is a pivotal carrier protein responsible for the exchange of ADP and ATP across the inner mitochondrial membrane—an essential step for oxidative phosphorylation and overall cellular energy homeostasis. ANT1 is highly expressed in heart and skeletal muscle, and its function is governed by specific substrate‐binding features and an alternating access mechanism that ensures efficient nucleotide transport. This fundamental bioenergetic role has been demonstrated by studies assessing its transport kinetics, structural determinants, and capacity to restore energy flux in model systems."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "10"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nApart from its role in bioenergetics, ANT1 is a crucial regulator of mitochondrial membrane permeability and apoptosis. It directly participates in the formation and regulation of the permeability transition pore by interacting with proteins such as cyclophilin D, and its function is modulated by post‐translational modifications—phosphorylation and acetylation of key residues—that alter its conformational dynamics. Such modifications can change its substrate binding and transport activity, thereby influencing apoptotic signaling cascades and cellular responses to oxidative stress. ANT1’s impact on programmed cell death and its interplay with other mitochondrial proteins have been shown to contribute to changes in mitochondrial ultrastructure and the execution of cell death programs under stress conditions."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "11", "end_ref": "25"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nGenetic mutations and aberrant regulation of SLC25A4/ANT1 are implicated in a broad spectrum of mitochondrial disorders, including autosomal‐dominant progressive external ophthalmoplegia, cardiomyopathy, and skeletal myopathies. Both dominant and recessive mutations impair ADP/ATP transport, leading to mitochondrial dysfunction, increased reactive oxygen species production, and destabilization of mitochondrial DNA maintenance. Moreover, altered ANT1 expression and its consequent effects on cellular apoptosis and metabolic remodeling underscore its potential as a biomarker and therapeutic target in clinical conditions marked by energy deficits and oxidative stress. Recent studies highlight its involvement in disease modulation and signal transduction pathways that contribute to pathogenesis in affected tissues."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "26", "end_ref": "41"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Xin Jie Chen "}, {"type": "b", "children": [{"type": "t", "text": "Induction of an unregulated channel by mutations in adenine nucleotide translocase suggests an explanation for human ophthalmoplegia."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Hum Mol Genet (2002)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1093/hmg/11.16.1835"}], "href": "https://doi.org/10.1093/hmg/11.16.1835"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "12140186"}], "href": "https://pubmed.ncbi.nlm.nih.gov/12140186"}]}, {"type": "r", "ref": 2, "children": [{"type": "t", "text": "Carine De Marcos Lousa, Véronique Trézéguet, Anne-Christine Dianoux, et al. 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