{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nSLC39A14, also known as ZIP14, is a versatile transmembrane metal‐ion transporter that plays a central role in cellular homeostasis by mediating the uptake of essential trace metals. Early studies demonstrated that ZIP14 actively imports zinc in a temperature‐dependent manner, and its cell surface expression is increased by pro‐inflammatory cytokines such as interleukin‐6, linking its regulation to the acute‐phase response and the resultant hypozincemia observed during infection and inflammation. Moreover, ZIP14 contributes to the cellular assimilation of non–transferrin‐bound iron via its localization within both plasma membranes and endosomal compartments. Additional work has revealed that ZIP14 can be alternatively spliced in malignant tissues, suggesting that distinct transcript variants might serve as biomarkers in cancers such as colorectal carcinoma.<br>."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "8"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn addition to its well‐documented role in zinc and iron uptake, SLC39A14 is pivotal for manganese transport. Loss‐of‐function mutations in SLC39A14 have been identified in patients with an autosomal recessive disorder characterized by systemic manganese accumulation, which manifests clinically as early‐onset parkinsonism–dystonia and neurodegeneration. Model systems including cellular assays in neuroblastoma cells and zebrafish have corroborated that ZIP14 mediates manganese uptake and that its dysregulation leads to abnormal manganese deposition in the brain. Furthermore, at the blood–brain barrier, ZIP14, together with its family member ZIP8, facilitates a bidirectional manganese flux critical for maintaining cerebral manganese balance. These insights underscore the transporter’s essential role not only in nutrient uptake but also in detoxification and the prevention of manganese‐induced neurotoxicity.<br>."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "9", "end_ref": "15"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its roles in trace metal uptake, SLC39A14 is increasingly recognized for its contributions to broader aspects of cellular and systemic metabolism. Genetic ablation and in-depth mechanistic studies in animal models have revealed that disruption of ZIP14 alters gastrointestinal metal absorption, perturbs hepatocyte regeneration, and impairs insulin signaling—all of which contribute to metabolic defects such as hypoglycemia and increased adiposity. Post‐translational modifications including N‐linked glycosylation and proteasome‐mediated degradation further fine‐tune the protein’s plasma membrane abundance, with regulatory inputs from factors such as the hereditary hemochromatosis protein HFE. In addition, emerging evidence links ZIP14 function to placental metal handling and to the pathogenesis of various malignancies including hepatocellular and renal cell carcinomas, while alterations in its expression in cardiac cells implicate it as a potential player in heart failure.<br>."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "16", "end_ref": "25"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "K M Taylor, H E Morgan, A Johnson, et al. 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"}, {"type": "b", "children": [{"type": "t", "text": "Interleukin-6 regulates the zinc transporter Zip14 in liver and contributes to the hypozincemia of the acute-phase response."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Proc Natl Acad Sci U S A (2005)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1073/pnas.0502257102"}], "href": "https://doi.org/10.1073/pnas.0502257102"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "15863613"}], "href": "https://pubmed.ncbi.nlm.nih.gov/15863613"}]}, {"type": "r", "ref": 3, "children": [{"type": "t", "text": "Ningning Zhao, Junwei Gao, Caroline A Enns, et al. 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