Target intelligence / Profile preview

Solute carrier family 30 member 9 (SLC30A9)

Target
SLC30A9
Molecular classification
Transporter, Mitochondrial zinc exporter, Solute carrier family (SLC transporter)
01

Overview

Solute carrier family 30 member 9 (SLC30A9) is a **mitochondrial zinc transporter** that exports Zn2+ from mitochondria to the cytosol, helping maintain intracellular zinc homeostasis and ensuring normal mitochondrial morphology and function[1][2][3][5][7]. SLC30A9 is localized to the mitochondrial membrane and operates as a proton-coupled zinc antiporter, utilizing the mitochondrial proton gradient to export zinc ions. Loss of SLC30A9 results in mitochondrial zinc overload, swelling, impaired mitochondrial metabolism, and is associated with neurodegenerative and developmental disorders, such as Birk-Landau-Perez syndrome. In addition to its main transporter function, SLC30A9 has minor roles as a nuclear receptor coactivator and may influence Wnt-responsive gene transcription. SLC30A9 is evolutionarily conserved and essential for organismal health[1][2][4][5][7].

Other names
ZnT-9Zinc transporter 9ZNT9Proton-coupled zinc antiporter SLC30A9, mitochondrialHuman embryonic lung proteinGRIP1-dependent nuclear receptor coactivatorC4orf1HUELGAC63BILAPES
02

Mechanism of action

Drugs targeting this molecule would likely act as **inhibitors or agonists** of mitochondrial zinc export activity, altering intracellular/mitochondrial zinc distribution; however, no approved or experimental drugs are specifically referenced in current literature[2][1][5].

03

Biological functions

Zinc ion homeostasisRegulation of mitochondrial morphologyZinc export from mitochondriaRegulation of mitochondrion organizationSecondary nuclear receptor coactivator (minor function)Transcriptional activation of Wnt-responsive genes (minor/nuclear function)
04

Disease associations

Neurodegenerative disease (mitochondrial dysfunction, neurodegeneration)Birk-Landau-Perez syndrome (cerebro-renal syndrome)Developmental disorders associated with mitochondrial dysfunctionPsychomotor regression-oculomotor apraxia-movement disorder-nephropathy syndrome
05

Safety considerations

Disruption of SLC30A9 leads to mitochondrial dysfunction, swelling, and neurotoxicityPotential neurodegeneration if SLC30A9 activity is inhibited too stronglyEffects on fertility due to altered zinc signaling in sperm activation (animal models)
06

Interacting drugs

None directly listed in current sources; no known small molecule modulators/approved drugs targeting SLC30A9 as of 2025[5][2][1].
07

Biomarkers

Elevated or depleted mitochondrial Zn2+ levels (potential biomarker in research, not used clinically)Mutational status of SLC30A9 in Birk-Landau-Perez syndrome

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