SLC30A2 Membrane Protein Introduction

Introduction of SLC30A2

Solute carrier family 30 member 2 (SLC30A2), also known as zinc transporter 2 (ZnT-2), is a protein that in humans is encoded by the SLC30A2 gene. It is a member of the ZnT family (ZnT1-10) that transport zinc from the cytosol, either across the cell membrane or into intracellular compartments.

Function of SLC30A2 Membrane Protein

SLC30A2 (ZnT2) was originally identified as a transporter protein that confers zinc-sensitive cells the ability to become zinc-resistant. Currently, it is known as a zinc transporter, and loss-of-function mutations cause transient neonatal zinc deficiency (TNZD). During the past years, a number of reports revealed that the expression of SLC30A2 is restricted to secretory cells, such as acinar pancreatic cells, prostate epithelial cells, placental trophoblasts, Paneth cells, and mammary epithelial cells (MECs). Studies have shown that SLC30A2 consists of six transmembrane domains with cytoplasmic N- and C-termini that contain numerous regulatory domains and functions as a dimer to transport zinc from the cytoplasm into vesicles. It has also been reported that the ability to increase SLC30A2 expression and vesicular zinc could protect cells from zinc cytotoxicity. What’s more, SLC30A2 variants are associated with abnormally low milk Zn levels and can lead to severe infantile Zn deficiency.

Fig.1 Proposed model of zinc transport and secretion in pancreatic acinar cells. (Guo, 2010)

Application SLC30A2 of Membrane Protein in Literature

1. Rivera O.C., et al. ZnT2 is critical for lysosome acidification and biogenesis during mammary gland involution. American Journal of Physiology-Regulatory, Integrative and Comparative Physiology. 2018, 315(2):R323-R335. PubMed ID: 29718697
   
   

   This article indicates that ZnT2 is a novel regulator of v-ATPase assembly, driving lysosome biogenesis, acidification and tissue remodeling during mammary gland involution.

2. Lee S., et al. A genetic variant in SLC30A2 causes breast dysfunction during lactation by inducing ER stress, oxidative stress, and epithelial barrier defects. Scientific reports. 2018, 8(1):3542. PubMed ID: 29476070
   
   

   This study confirms that ZnT2 is important for normal breast function in women during lactation, and suggests that women who harbor defective variants in ZnT2 may be at-risk for poor lactation performance.

3. Itsumura N., et al. Novel mutations in SLC30A2 involved in the pathogenesis of transient neonatal zinc deficiency. Pediatric research. 2016, 80(4):586. PubMed ID: 27304099
   
   

   This article indicates that many SLC30A2/ZnT2 mutations cause or potentially cause transient neonatal zinc deficiency.

4. Alam S., et al. Exome sequencing of SLC30A2 identifies novel loss-and gain-of-function variants associated with breast cell dysfunction. Journal of mammary gland biology and neoplasia. 2015, 20(3-4):159-72. PubMed ID: 26293594
   
   

   This article indicates that SLC30A2 variants are common in dysregulated Zn management and can lead to breast cell dysfunction. This suggests that genetic variation in ZnT2 could be an important modifier of infant growth/development and reproductive health/disease. Importantly, milk [Zn] level may serve as a bio-reporter of breast function during lactation.

5. Lee S., et al. Essential role for ZnT2-mediated zinc transport in mammary gland development and function during lactation. Journal of Biological Chemistry. 2015, 290(21):13064-78. PubMed ID: 25851903
   
   

   This report demonstrates that ZnT2-mediated zinc transport is critical for mammary gland function, indicating that defects in ZnT2 not only reduce milk zinc concentration but may compromise breast health and increase the risk for lactation insufficiency in lactating women.

SLC30A2 Preparation Options

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Reference

1. Guo, et al. (2010). STAT5-glucocorticoid receptor interaction and MTF-1 regulate the expression of ZnT2 (Slc30a2) in pancreatic acinar cells. Proceedings of the National Academy of Sciences. 290(21):13064-78.

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