{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nThe secretin receptor (SCTR) is a class B G protein‐coupled receptor that mediates the actions of its natural ligand secretin in multiple organ systems. In the liver it plays a pivotal role in cholangiocyte physiology, where enhanced SCTR signaling contributes to cholangiocyte proliferation, activation of fibrogenic pathways, and the progression of cholestatic injury and conditions such as primary sclerosing cholangitis and primary biliary cholangitis. In the pancreas and biliary tree, SCTR regulates bicarbonate and fluid secretion, and its differential coupling to cyclic AMP signaling underlies mitogenic responses in normal cholangiocytes while, in cholangiocarcinoma cells, secretin can have an antiproliferative effect. SCTR expression is also noted in neural tissues such as the cerebellum and has been linked to potential roles in food intake and metabolic regulation."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "6"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nStructural and molecular investigations have revealed critical insights into SCTR function. Biophysical studies, including cryo-electron microscopy and molecular dynamics simulations, have delineated the receptor’s unique extracellular domain arrangement and the extended interactions formed with secretin that drive receptor activation. Structure–activity analyses using cysteine trapping and lactam-constrained peptide analogues have defined key interactions within extracellular loops and transmembrane helices. Furthermore, studies have shown that SCTR can associate with receptor activity–modifying protein 3 (RAMP3) and exists as highly specific homo-dimers (with no evidence for higher-order oligomers), while regulatory mechanisms at the transcriptional level involve Sp1/Sp3 interactions and epigenetic control via promoter methylation and neuron restrictive silencer factor."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "7", "end_ref": "16"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nAberrant SCTR expression and function play significant roles in various malignancies. In the liver and pancreas, altered SCTR expression—including the appearance of splice variants that may act in a dominant negative manner—has been linked to altered proliferative responses and tumor progression. In non-neoplastic tissues, such as the normal pancreas and liver, robust SCTR expression underpins physiological secretin actions; however, in cancers (including cholangiocarcinoma, pancreatic, colorectal, breast, and lung tumors) SCTR dysregulation, often associated with epigenetic modifications, has been proposed as a useful diagnostic and therapeutic target."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "17", "end_ref": "26"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nRecent studies also highlight that SCTR can form functional cross-class receptor complexes. For instance, interactions between SCTR and the angiotensin receptor have been shown to modulate secretin-stimulated cyclic AMP responses through allosteric mechanisms, suggesting that receptor crosstalk may fine-tune physiological outcomes and represent novel targets for therapeutic intervention in metabolic diseases."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "27"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Nan Wu, Fanyin Meng, Pietro Invernizzi, et al. 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