{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\n Placental protein 13 (PP13), encoded by the LGALS13 gene and also known as galectin‑13, is a placenta‐specific lectin that is predominantly expressed in syncytiotrophoblast cells. Structural studies have defined its typical “jellyroll” β‑sandwich fold and revealed that, unlike many prototype galectins, it dimerizes through unique disulfide bridges and exhibits an altered carbohydrate‐recognition domain (for example, a key residue substitution at position 53) that confers distinct sugar‐binding and hemagglutination properties (see."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "4"}]}, {"type": "t", "text": " Functionally, LGALS13 is secreted via a non‑classical ectocytotic pathway—in association with extracellular vesicles—and interacts with proteins such as annexin II and actin; these interactions are thought to help establish specialized immune “zones” at the feto‑maternal interface that promote trophoblast invasion as well as uteroplacental vascular remodeling (see."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "5"}]}, {"type": "t", "text": " In addition, altered expression or genetic variants of LGALS13 have been strongly associated with adverse pregnancy outcomes—most notably preeclampsia—making PP13 a promising early biomarker for placental dysfunction; indeed, reduced first‐trimester PP13 levels and decreased placental mRNA expression of LGALS13 have been linked to disease severity (see."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "7", "end_ref": "10"}]}, {"type": "t", "text": " Moreover, mutations or truncations that disrupt its dimerization or nuclear trafficking—such as variants that prevent its normal cellular distribution—may underlie the pathogenic mechanisms leading to preeclampsia (see."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "11"}]}, {"type": "t", "text": " Collectively, these findings indicate that LGALS13/galectin‑13 functions as a critical immunomodulatory and vascular‑regulatory factor in normal placental development, while its dysregulation contributes to placental disorders.\n "}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Nandor G Than, Elah Pick, Szabolcs Bellyei, et al. 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"}, {"type": "b", "children": [{"type": "t", "text": "Galectin-13, a different prototype galectin, does not bind β-galacto-sides and forms dimers via intermolecular disulfide bridges between Cys-136 and Cys-138."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Sci Rep (2018)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1038/s41598-018-19465-0"}], "href": "https://doi.org/10.1038/s41598-018-19465-0"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "29343868"}], "href": "https://pubmed.ncbi.nlm.nih.gov/29343868"}]}, {"type": "r", "ref": 4, "children": [{"type": "t", "text": "Jiyong Su, Linlin Cui, Yunlong Si, et al. 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