{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nSLC29A3 encodes the human equilibrative nucleoside transporter‐3 (hENT3), a protein principally located on intracellular membranes such as lysosomes—and, in select cell types, mitochondria and the cell surface—that mediates the transport of endogenous nucleosides and nucleoside analog drugs. Functional studies have demonstrated that hENT3 exhibits broad substrate selectivity with low affinity and is distinguished by a strong pH dependence (optimal activity near pH 5.5), a property that mirrors its acidic subcellular compartment localization and contributes to nucleoside‐drug transport that is relatively insensitive to classical inhibitors. This transporter also plays a role in the mitochondrial uptake of drugs known for their mitochondrial toxicity."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "4"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nMutations in SLC29A3 have been implicated in a spectrum of autosomal recessive, multisystem disorders. Several studies have linked pathogenic variants of SLC29A3 to clinical syndromes that include H syndrome, pigmented hypertrichosis with insulin‐dependent diabetes (PHID) syndrome, familial forms of histiocytosis (including Rosai–Dorfman disease and Faisalabad histiocytosis), and dysosteosclerosis. Affected patients typically present with cutaneous hyperpigmentation and hypertrichosis, variable endocrinopathies (such as diabetes and hypogonadism), skeletal dysplasias, hepatosplenomegaly, and other organ anomalies. Notably, alternative splicing events—normally leading to noncoding transcripts—can, in the presence of frameshift mutations, produce hypomorphic isoforms that partially rescue transporter function and may account for atypically mild phenotypes. Collectively, these findings underscore the pleiotropic impact of hENT3 dysfunction on cellular metabolism and tissue homeostasis."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "5", "end_ref": "19"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nEmerging research also suggests that SLC29A3 plays roles in oncogenesis and drug response. Genetic polymorphisms in SLC29A3 have been associated with overall survival differences in patients with non‐small cell lung cancer, while altered expression—mediated by microRNAs—is implicated in the progression of rectal cancer. In addition, novel mutations in regulatory (untranslated) regions have been linked to phenotypes related to PHID syndrome. These studies point to SLC29A3 as a promising prognostic biomarker and potential therapeutic target in cancer, with implications for refining treatment strategies based on individual genetic variability."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "20", "end_ref": "25"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nFinally, mechanistic insights have revealed that loss‐of‐function mutations in SLC29A3 can lead to the abnormal activation of nucleoside‐sensing toll‐like receptors and downstream MAPK signaling pathways, thereby promoting inflammatory histiocytosis. This novel understanding of hENT3’s role in linking defective lysosomal nucleoside transport to inflammation has important therapeutic implications, as treatment with MEK inhibitors has shown promise in ameliorating disease manifestations."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "26"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Stephen A Baldwin, Sylvia Y M Yao, Ralph J Hyde, et al. 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