{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nRecent investigations have revealed a critical role for miR-3606‐3p in modulating fibrotic signaling in systemic sclerosis. In fibroblasts, miR-3606-3p directly binds to the 3′-UTR of the TGF-β type II receptor (TGFBR2) mRNA, thereby downregulating its expression. This reduction in TGFBR2 levels leads to decreased SMAD2/3 activation, diminished type I collagen synthesis, and inhibition of fibroblast cell cycle progression. Notably, systemic sclerosis dermal tissues and primary fibroblasts exhibit reduced levels of miR-3606-3p, suggesting that insufficient miR-3606-3p may contribute to the hyperactive TGF-β signaling observed in the disease."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "1"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn contrast, other studies in this collection have focused on glycosyltransferases—such as WBSCR17 and GALNT17—that contribute to dynamic membrane trafficking, endocytosis, and neurodevelopment. These investigations, performed on cellular and animal models, highlight the importance of post-translational modifications, particularly O-linked glycosylation, in controlling cell adhesion, signaling, and neural connectivity. Although these glycosylation-related genes (located in or near the Williams-Beuren syndrome and AUTS2 critical regions) impact diverse cellular processes, the function of miR-3606-3p is distinct in that it specifically attenuates TGF-β signaling through TGFBR2 repression. This juxtaposition underscores the multifaceted regulation of cellular homeostasis, with miR-3606-3p serving as a promising therapeutic target for fibrosis, while glycosylation enzymes more broadly influence membrane dynamics and neurological function."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "2", "end_ref": "4"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Xiangguang Shi, Qingmei Liu, Na Li, et al. 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"}, {"type": "b", "children": [{"type": "t", "text": "A putative polypeptide N-acetylgalactosaminyltransferase/Williams-Beuren syndrome chromosome region 17 (WBSCR17) regulates lamellipodium formation and macropinocytosis."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "J Biol Chem (2012)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1074/jbc.M112.370932"}], "href": "https://doi.org/10.1074/jbc.M112.370932"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "22787146"}], "href": "https://pubmed.ncbi.nlm.nih.gov/22787146"}]}, {"type": "r", "ref": 3, "children": [{"type": "t", "text": "P Anne Weisner, Chih-Ying Chen, Younguk Sun, et al. "}, {"type": "b", "children": [{"type": "t", "text": "A Mouse Mutation That Dysregulates Neighboring "}, {"type": "a", "children": [{"type": "t", "text": "i"}], "href": "i"}, {"type": "t", "text": "Galnt17"}, {"type": "a", "children": [{"type": "t", "text": "/i"}], "href": "/i"}, {"type": "t", "text": " and "}, {"type": "a", "children": [{"type": "t", "text": "i"}], "href": "i"}, {"type": "t", "text": "Auts2"}, {"type": "a", "children": [{"type": "t", "text": "/i"}], "href": "/i"}, {"type": "t", "text": " Genes Is Associated with Phenotypes Related to the Human AUTS2 Syndrome."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "G3 (Bethesda) (2019)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1534/g3.119.400723"}], "href": "https://doi.org/10.1534/g3.119.400723"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "31554716"}], "href": "https://pubmed.ncbi.nlm.nih.gov/31554716"}]}, {"type": "r", "ref": 4, "children": [{"type": "t", "text": "Chih-Ying Chen, Christopher H Seward, Yunshu Song, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Galnt17 loss-of-function leads to developmental delay and abnormal coordination, activity, and social interactions with cerebellar vermis pathology."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Dev Biol (2022)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1016/j.ydbio.2022.08.002"}], "href": "https://doi.org/10.1016/j.ydbio.2022.08.002"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "36002036"}], "href": "https://pubmed.ncbi.nlm.nih.gov/36002036"}]}]}]}