{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nSLCO1A2 encodes the organic anion‐transporting polypeptide 1A2 (OATP1A2), a versatile uptake transporter that is broadly expressed in human tissues—including the brain capillaries, intestinal epithelium, kidney, liver, retina, and even in certain tumor types—and facilitates the cellular entry of a wide range of endogenous molecules and drugs. OATP1A2 mediates the transport of compounds such as estrone 3‐sulfate, imatinib, fexofenadine, various anticancer agents (e.g. doxorubicin and taxanes), triptans for migraine, and even all‐trans‐retinol into specialized tissues. Its activity is often pH‐dependent and can be modulated by post‐translational events, which collectively underscore its key role in absorption, distribution, blood–brain barrier penetration and even in pathological states such as breast cancer and neurodegeneration."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "15"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nNumerous studies have demonstrated that genetic variation within SLCO1A2 can have profound effects on transporter function, with single nucleotide polymorphisms sometimes leading to altered transporter kinetics through impaired plasma membrane targeting, changes in glycosylation patterns, or disruption of intracellular regulatory interactions. In vitro investigations have shown that naturally occurring missense variants and polymorphisms within critical domains (including regions such as the sixth transmembrane segment and miRNA‐binding sites in the 3′‐UTR) can reduce the uptake capacity for substrates including estrone 3‐sulfate, imatinib, methotrexate, and fexofenadine. Such alterations in transporter performance have been linked in clinical settings to inter‐individual variability in drug disposition, altered therapeutic efficacy and toxicity, and may even influence disease risk or progression in conditions such as gallstone formation and breast cancer."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "16", "end_ref": "30"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn addition to genetic variation, SLCO1A2 function is subject to regulation by multiple intracellular signaling pathways and modulatory proteins. Studies have shown that kinase pathways such as those involving AMPK, as well as epigenetic modifications mediated by histone deacetylases (for example, HDAC6) and PDZ-domain adaptor proteins (PDZK1 and NHERF1), can influence OATP1A2 trafficking, membrane stability and recycling. These regulatory mechanisms further modulate substrate uptake and may have clinical implications in diverse settings ranging from altered drug–drug interactions and variable chemotherapeutic responses (e.g. celiprolol and imatinib) to potential roles in neurodegenerative disease and cancer prognosis."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "31", "end_ref": "38"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Wooin Lee, Hartmut Glaeser, L Harris Smith, et al. 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