{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nMIA3, which encodes the protein TANGO1, plays a central role in the organization of the early secretory pathway by orchestrating the export of bulky cargos such as procollagens from the endoplasmic reticulum (ER). TANGO1 achieves this by scaffolding ER exit sites and corralling COPII coat components as well as recruiting specialized membranes—including those from the ER–Golgi intermediate compartment—to generate enlarged transport carriers that are capable of exporting large cargo. Disruption of TANGO1 function impairs these processes, leading to defects in collagen secretion and general alterations in secretory pathway organization that contribute to a spectrum of connective tissue and fibrotic disorders."}, {"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": "\nIn addition to its pivotal role in ER export, MIA3/TANGO1 exhibits context‐dependent functions in tumor biology and cell adhesion. In several malignancies—including melanoma, colon, and oral squamous cell carcinoma—the loss or down‐regulation of MIA3 has been associated with enhanced cell motility and invasiveness, supporting its tumor‐suppressive activity. Conversely, in hepatocellular carcinoma, TANGO1 can promote tumor progression by interacting with signaling mediators to activate the PI3K/AKT/mTOR pathway and by modulating cellular redox status through factors such as CHAC1. Moreover, evidence indicates that MIA3 may regulate integrin activity—as exemplified by its interaction with the leukocyte‐specific CD11c receptor—to influence monocyte adhesion and migration."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "11", "end_ref": "16"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nGenetic studies have repeatedly implicated variants in MIA3 in cardiovascular disease risk. Genome‐wide association studies and follow‐up analyses have associated MIA3 single nucleotide polymorphisms with myocardial infarction and coronary heart disease, suggesting that perturbation of MIA3 function—likely through its impact on ER export of extracellular matrix components—may alter endothelial cell function and vascular homeostasis. Moreover, analyses in diverse populations and in conditions such as rheumatoid arthritis and even Moyamoya disease indicate that MIA3 genetic variation may influence not only cardiovascular phenotypes but also inflammatory and metabolic processes that contribute to disease pathogenesis."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "17", "end_ref": "28"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "António J M Santos, Ishier Raote, Margherita Scarpa, et al. 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