Target intelligence / Profile preview

Solute carrier family 30 member 7 (SLC30A7 (commonly ZnT7))

Target
SLC30A7 (commonly ZnT7)
Molecular classification
Transporter, Ion transporter, Solute carrier family (SLC family)
01

Overview

Solute carrier family 30 member 7 (SLC30A7, ZnT7) is a *zinc transporter protein* localized primarily in the Golgi membrane and other organelles along the secretory pathway[1][3][4]. Its main function is to mediate active export of Zn²⁺ ions from the cytosol into the lumen of Golgi and secretory vesicles, utilizing a Zn²⁺/H⁺ antiport mechanism[1][4]. This activity is critical for the incorporation of zinc into newly synthesized enzymes, maintenance of intracellular zinc homeostasis, and prevention of cytosolic zinc toxicity[2][3]. SLC30A7 is essential for diverse physiological processes, including proper protein folding, cell survival signaling, and development. Genetic mutations in SLC30A7 are causatively linked to rare developmental disorders such as Joubert syndrome, growth deficiencies, testicular and hematologic defects, and may contribute to tumor progression in experimental models due to cellular zinc deficiency and activation of stress signaling pathways[2][3]. No drugs currently target SLC30A7 directly, and modulation of its function presents significant therapeutic and safety challenges because of zinc’s universal biological roles.

Other names
Zinc transporter 7ZnT7ZNT7ZNT-7ZNTL2ZnT-7ZnTL2Znt-like transporter 2ZHSzinc transporter like 2Solute carrier family 30 (zinc transporter), member 7zinc transporter ZnT-7
02

Mechanism of action

Drugs that might target this transporter would likely act by modulating zinc efflux from cytosol to the Golgi/secretory organelles, thereby affecting zinc-dependent biochemical processes and signaling[1][4].

03

Biological functions

Zinc ion homeostasisTransmembrane zinc ion transport (export of Zn2+ from cytosol into Golgi and secretory pathway organelles)Regulation of protein folding and activation (via ensuring zinc supply to zinc-dependent enzymes)Modulation of cell survival pathways (through PI3K/AKT signaling under cellular stress)Influence on apoptosis and autophagy
04

Disease associations

Developmental disorders (including Joubert syndrome)Syndromic phenotypes (stunted growth, testicular hypoplasia, bone marrow failure)Neurodevelopmental disorders (prominent forehead, feeding difficulties)Tumor growth and invasion (through zinc deficiency-induced ER stress and JNK signaling)Ziegler-Huang syndrome
05

Safety considerations

Disrupted SLC30A7 function can cause systemic zinc imbalance, contributing to developmental defects, bone marrow failure, and increased susceptibility to certain stress responses[2][3].Therapeutic modulation may risk global zinc dysregulation, affecting multiple organ systems and enzymatic pathways[4].
06

Interacting drugs

No approved or clinically established drugs are currently known to directly target SLC30A7 or ZnT7 in humans[3].
07

Biomarkers

Changes in SLC30A7 expression or loss-of-function mutations may serve as *potential* biomarkers for disorders of zinc metabolism, Joubert syndrome, syndromic growth failure, or tumor aggressiveness[2][3]. However, validated clinical biomarkers are not established.

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