{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,29]],"date-time":"2026-08-29T08:41:22Z","timestamp":1787992882458,"version":"build-2784847793"},"reference-count":51,"publisher":"Public Library of Science (PLoS)","issue":"4","license":[{"start":{"date-parts":[[2026,4,17]],"date-time":"2026-04-17T00:00:00Z","timestamp":1776384000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["81873686"],"award-info":[{"award-number":["81873686"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100019092","name":"Science Fund for Distinguished Young Scholars of Hunan Province","doi-asserted-by":"publisher","award":["2023JJ30715"],"award-info":[{"award-number":["2023JJ30715"]}],"id":[{"id":"10.13039\/501100019092","id-type":"DOI","asserted-by":"publisher"}]},{"name":"Scientific Research Project of Hunan Provincial Health Commission","award":["A202303018385"],"award-info":[{"award-number":["A202303018385"]}]},{"name":"Health Research Project of Hunan Provincial Health Commission","award":["W20243024"],"award-info":[{"award-number":["W20243024"]}]},{"name":"Distinguished Professor of the Lotus Scholars Award Program of Hunan Province"},{"name":"Wisdom Accumulation and Talent Cultivation Project of the Third Xiangya Hospital of Central South University","award":["YX202109"],"award-info":[{"award-number":["YX202109"]}]},{"DOI":"10.13039\/501100012476","name":"Fundamental Research Funds for Central Universities of the Central South University","doi-asserted-by":"publisher","award":["2023ZZTS0335"],"award-info":[{"award-number":["2023ZZTS0335"]}],"id":[{"id":"10.13039\/501100012476","id-type":"DOI","asserted-by":"publisher"}]},{"name":"Sublimation Scholars Project of Central South University"}],"content-domain":{"domain":["www.plosone.org"],"crossmark-restriction":false},"short-container-title":["PLoS One"],"abstract":"<jats:p>\n                    Primary brain calcification (PBC) is a rare neurodegenerative disease featured by bilateral brain calcifications and exhibiting high phenotypic and genetic heterogeneity. The clinical manifestations mainly include movement disorders, cognitive deficits, and neuropsychiatric symptoms. In this study, a novel heterozygous nonsense variant, c.1669C\u2009&gt;\u2009T [p.(Gln557*)], in the solute carrier family 20 member 2 gene (\n                    <jats:italic>SLC20A2<\/jats:italic>\n                    ), encoding type III sodium-dependent inorganic phosphate transporter 2 (PiT2), was identified in a Han-Chinese family with PBC using whole exome sequencing and Sanger sequencing. Bioinformatics analysis predicted the variant\u2019s deleterious effect. The cellular function impacts of the p.Gln557* variant and three other common PBC-related\n                    <jats:italic>SLC20A2<\/jats:italic>\n                    variants, p.Ser113*, p.Ala585Thr, and p.Ser601Trp, were subsequently revealed. Subcellular localization analysis showed that the PiT2-Q557*, A585T, and S601W mutants mainly distributed in the plasma membrane and cytosol, whereas the PiT2-S113* mutant showed a diffuse distribution throughout the cells. All four investigated variants significantly impaired cellular inorganic phosphate transport activity. The protein mislocalization-inducing p.Ser113* variant likely causes haploinsufficiency, while the p.Gln557*, p.Ala585Thr, and p.Ser601Trp variants may lead to full or partial loss of function, or exert a dominant-negative effect. Cells expressing PiT2 mutants all exhibited inhibited proliferative and migratory activities, along with enhanced apoptosis. These\n                    <jats:italic>SLC20A2<\/jats:italic>\n                    variants probably impair critical cellular functions, potentially providing an explanation for the neurological symptoms observed in PBC patients. These findings further broaden\n                    <jats:italic>SLC20A2<\/jats:italic>\n                    variant spectrum and provide valuable mechanistic insights into the pathogenesis of\n                    <jats:italic>SLC20A2<\/jats:italic>\n                    -associated PBC.\n                  <\/jats:p>","DOI":"10.1371\/journal.pone.0346635","type":"journal-article","created":{"date-parts":[[2026,4,17]],"date-time":"2026-04-17T17:46:55Z","timestamp":1776448015000},"page":"e0346635","update-policy":"https:\/\/doi.org\/10.1371\/journal.pone.corrections_policy","source":"Crossref","is-referenced-by-count":1,"title":["A novel SLC20A2 nonsense variant and mechanistic studies of primary brain 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