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ZIP10 (Solute carrier family 39 member 10) is a transmembrane zinc transporter that facilitates the influx of zinc ions into the cytoplasm from the extracellular space or intracellular organelles [1.2.2, 1.5.1]. It plays a critical role in the immune system, particularly in B-cell development and survival, by inhibiting caspase activity and modulating B-cell receptor (BCR) signaling [1.1.1, 1.1.3]. In oncology, ZIP10 is frequently overexpressed in cancers such as breast cancer and lung adenocarcinoma, where it often forms a functional heterodimer with ZIP6 to promote mitosis and the epithelial-to-mesenchymal transition (EMT) [1.2.2, 1.3.1, 1.4.3]. Beyond cancer and immunity, ZIP10 is essential for epidermal homeostasis through the regulation of histone acetyltransferase activity and for erythropoiesis by supporting heme synthesis under zinc-limited conditions [1.1.4, 1.2.3]. Therapeutic strategies targeting ZIP10, including the development of monoclonal antibodies, aim to disrupt zinc-dependent oncogenic signaling and sensitize tumors to treatments like radiotherapy [1.3.1, 1.4.3]. However, therapeutic intervention must account for potential safety concerns, such as impaired B-cell function, skin barrier defects, and anemia, given the transporter's widespread physiological importance [1.1.1, 1.2.3, 1.4.2]. Genetic variants in the SLC39A10 gene have also been identified as potential biomarkers for anemia risk and hematological health [1.2.3, 1.4.1]. Overall, ZIP10 represents a versatile target for addressing malignancies and immune-related disorders through the modulation of cellular zinc homeostasis [1.4.3, 1.5.1].
Zinc influx inhibition and disruption of ZIP6/ZIP10 heterodimerization
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