{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nSLC6A6, which encodes the taurine transporter (TauT), is a sodium‐ and chloride‐dependent, high‐affinity membrane protein that mediates the uptake of taurine—a β‐amino acid indispensable for antioxidant defense, osmoregulation, and cell signaling. It is prominently expressed in epithelial tissues such as the intestinal brush‐border membrane where it ensures efficient taurine absorption at low substrate concentrations, and it is vital in kidney and placental cells for proper development and cell survival. In these organs TauT expression is controlled by key transcriptional regulators including p53 and WT1, which link its levels to developmental and stress‐responsive pathways ["}, {"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": "\nSLC6A6 expression is dynamically regulated by a host of physiological and pathological stimuli. In intestinal epithelial cells, inflammatory cytokines such as tumor necrosis factor–α (TNF‐α) markedly enhance TauT transcription and activity, as shown by kinetic studies in Caco‐2 cells ["}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "6", "end_ref": "8"}]}, {"type": "t", "text": "]. In parallel, oxidative and hyperglycemic stress—as encountered in retinal pigment epithelial and Schwann cells—modulates TauT levels, while differences in taurine transporter activity have been documented in fetal T lymphocytes, indicating implications for intrauterine development ["}, {"type": "fg", "children": [{"type": "fg_f", "ref": "9"}]}, {"type": "t", "text": "]. In the kidney, TauT deficiency has been linked to impaired cell-cycle progression and abnormal renal development, whereas increased TauT expression protects proximal tubular cells from cisplatin-induced apoptosis. Moreover, in diabetic models TauT is upregulated in circulating mononuclear cells, a change that appears related to alterations in oxidative stress, while in the placenta reduced TauT activity—potentially mediated by nitric oxide—and dysregulation by vitamin D₃/retinoic acid contribute to compromised trophoblast renewal and fetal growth restriction. Additional studies have reported modulation of TauT under osmotic stress in chondrocytes and have connected its deficiency to early retinal degeneration and to changes observed in diabetic retinopathy; in pregnancies complicated by pre-eclampsia or obesity, altered transporter activity may further impair placental function ["}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "11", "end_ref": "22"}]}, {"type": "t", "text": "].\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its fundamental physiological roles, SLC6A6 has emerged as a promising target in oncology and as a candidate biomarker in diverse disease settings. For example, the transporter mediates the uptake of δ‑aminolevulinic acid in cancer cells, thereby enhancing protoporphyrin accumulation and the efficacy of photodynamic therapy. In parallel, novel monoclonal antibodies have been generated against extracellular epitopes of TauT in metastatic breast cancer cells, providing a potential avenue for targeted therapeutics. Aberrant SLC6A6 expression has also been correlated with aggressive phenotypes in gastric cancer, and integrative reviews emphasize how protein kinase–dependent phosphorylation events regulate osmolyte transporters under stress conditions ["}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "23", "end_ref": "26"}]}, {"type": "t", "text": "].\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Catriona M H Anderson, Alison Howard, Julian R F Walters, et al. 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