{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nRNASET2, a highly conserved member of the T2 ribonuclease family, plays a crucial role in RNA turnover and innate immune activation. Its acid endoribonuclease activity is essential for degrading RNA substrates in lysosomes and within the mitochondrial intermembrane space, thereby maintaining cellular RNA homeostasis. In addition, RNASET2 contributes to immune sensing by cleaving complex single‐stranded RNAs to generate specific degradation products that act as agonistic ligands for Toll‐like receptor 8 (TLR8), linking RNA catabolism to innate immune signaling."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "4"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn developmental and autoimmune contexts, RNASET2 has emerged as a key factor influencing both neurodevelopment and immune regulation. Loss‐of‐function mutations in the RNASET2 gene are linked to infantile cystic leukoencephalopathy—a neurodegenerative condition characterized by cortical cysts and multifocal white matter lesions that arise from impaired lysosomal degradation of RNA in neurons. Moreover, genetic association studies have identified RNASET2 as part of risk loci for autoimmune diseases such as vitiligo and thyroid disorders. In these settings, stress conditions (from UV irradiation, oxidative stress, or inflammatory factors) induce RNASET2 expression in melanocytes and keratinocytes, promoting apoptosis via the TRAF2–caspases pathway and suggesting that RNASET2 functions as an “alarm” signal in modulating immune responses."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "5", "end_ref": "12"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its roles in RNA metabolism and immune regulation, RNASET2 exerts multifaceted functions in tumor suppression, cellular stress responses, and tissue remodeling. In several cancer models—including ovarian, melanoma, and renal cell carcinoma—RNASET2 acts as a tumor antagonist by both cell‐autonomous mechanisms (such as modulating cytoskeletal organization, inhibiting proliferation, and impairing migratory and invasive capacities) and non–cell‐autonomous mechanisms (for example, by recruiting M1‐polarized macrophages to the tumor microenvironment). Its tumor‐suppressive activity may occur independently of its ribonuclease function, as suggested by studies showing that engineered, catalytically inactive forms retain the ability to bind actin and inhibit angiogenesis. In addition, RNASET2 is implicated in the regulation of drug resistance and is modulated by ubiquitin-mediated proteasomal degradation. Notably, aberrant RNASET2 expression has also been correlated with reduced sperm motility—likely by interfering with key signaling pathways such as PKA/PI3K/calcium cascades—as well as with alterations in splice variant expression that influence aggressive tumor behavior. Collectively, these diverse functions underline RNASET2 as a critical regulator in cancer biology, reproductive health, and overall cellular homeostasis."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "13", "end_ref": "35"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Noémie Haud, Firat Kara, Simone Diekmann, et al. 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