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Zinc transporter 1 (ZnT1), encoded by the SLC30A1 gene, is a ubiquitous transmembrane protein and the primary exporter of zinc from the cytoplasm to the extracellular space [1.1.1, 1.3.4]. It is essential for maintaining cellular zinc homeostasis and protecting cells from zinc toxicity [1.1.5, 1.3.4]. Beyond its role in zinc transport, ZnT1 has been found to transport copper and interact with other signaling molecules, such as NMDA receptors and L-type calcium channels, thereby influencing neuronal excitability and calcium signaling [1.3.1, 1.3.2]. In disease contexts, ZnT1 is frequently dysregulated; its overexpression is associated with poor prognosis in several cancers, while its loss of function can lead to impaired metal homeostasis and increased susceptibility to oxidative stress [1.1.1, 1.3.1]. Therapeutic interest in ZnT1 is growing, with research exploring small-molecule modulators, RNA interference, and antibody-based approaches to treat conditions like cancer, Wilson disease, and neurodegenerative disorders [1.2.1, 1.3.1]. However, targeting ZnT1 presents challenges due to its critical role in systemic zinc balance and potential for off-target effects in the gut and brain [1.2.2, 1.3.1].
Modulation of zinc efflux to regulate intracellular metal concentrations and downstream signaling pathways [1.2.1, 1.2.4].
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