{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nSLC10A1 encodes the sodium taurocholate cotransporting polypeptide (NTCP), a multi‐transmembrane carrier expressed almost exclusively in hepatocytes that mediates the sodium‐dependent uptake of bile acids from portal blood. This transport activity is crucial for maintaining bile acid homeostasis and ensuring proper enterohepatic circulation. NTCP function is tightly regulated at the transcriptional level by nuclear receptors (for example, the glucocorticoid receptor) and can be modulated by bile acids themselves, influencing both its expression and trafficking to the plasma membrane."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "5"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn addition to its primary role in bile acid transport, NTCP functions as a bona fide receptor for hepatitis B and D viruses (HBV and HDV). The virus–host interaction is mediated principally by the binding of the viral pre‑S1 domain to the extracellular region of NTCP, a determinant that overlaps with the substrate recognition site. Consequently, NTCP expression endows otherwise non‑permissive cells with susceptibility to HBV/HDV infection, while genetic or pharmacological interference with NTCP function can block viral entry and modify the efficiency of infection."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "6", "end_ref": "22"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nFurthermore, genetic variability and post‑translational regulation of SLC10A1 contribute to inter‐individual differences in NTCP function. Polymorphisms—including the clinically significant S267F substitution—and adaptive evolutionary changes at key amino acid residues can markedly alter bile acid transport efficiency as well as HBV receptor activity, thereby influencing clinical outcomes such as hypercholanemia, susceptibility to chronic HBV infection, and progression of liver disease. In addition, NTCP function is affected by its oligomerization state, interactions with other membrane proteins (for example, E‑cadherin), and signaling pathways that modulate its surface expression. These insights underscore NTCP’s dual role in physiology and pathophysiology and suggest that targeting its regulatory mechanisms may offer therapeutic potential in treating HBV infection and related liver disorders."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "23", "end_ref": "33"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Richard H Ho, Brenda F Leake, Richard L Roberts, et al. 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