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Showing SLC30A2 — ZNT2 is a alias.

SLC30A2

Proton-coupled zinc antiporter SLC30A2 · UniProt Q9BRI3

Length
372 aa
Mass
40.6 kDa
Annotated
2026-06-10
38 papers in source corpus 23 papers cited in narrative 23 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 6/6 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

SLC30A2/ZnT2 is a proton-coupled zinc antiporter (2H+/Zn2+ stoichiometry) that uses the V-ATPase-generated proton motive force to sequester cytosolic zinc into acidic intracellular compartments, protecting cells from zinc toxicity and supplying zinc to secretory granules (PMID:8617223, PMID:30893306). It localizes to endosomal/lysosomal vesicles, and through an N-terminal histidine-rich motif (51HHXH54) also targets the inner mitochondrial membrane to import zinc into mitochondria (PMID:21289295); alternatively spliced isoforms partition between secretory compartments and the plasma membrane (PMID:19496757). ZnT2 functions as a homodimer, and mutations that abolish dimerization or transport (W152R), destabilize the protein (S296L), or cause aggresomal/ER-Golgi mislocalization (H54R, G87R) reduce milk zinc and cause transient neonatal zinc deficiency, with G87R acting dominant-negatively over wild-type protein (PMID:17065149, PMID:22733820, PMID:23741301). In specialized secretory cells ZnT2 loads zinc into zymogen granules of pancreatic acini, Paneth cell and mast cell granules, and milk secretory vesicles, where it supports granule integrity, bactericidal function, innate immune signaling, and wound healing through a GPR39/IL-6 axis (PMID:20133611, PMID:28174721, PMID:31346193). ZnT2 expression is transcriptionally driven by prolactin via JAK2/STAT5 and by glucocorticoid/zinc-responsive elements, and post-translationally tuned by ubiquitination at N-terminal lysines K4/K6 and by TNFα-triggered dephosphorylation of S296 that unmasks a dileucine (L294L) AP-3 binding motif redirecting ZnT2 to lysosomes (PMID:19494234, PMID:20133611, PMID:25016022, PMID:25808614). This lysosomal zinc loading drives V-ATPase assembly and lysosome biogenesis and powers lysosomal-mediated cell death during mammary gland involution, and ZnT2 is required for normal mammary differentiation and lactation (PMID:25620235, PMID:25851903, PMID:29718697).

Mechanistic history

Synthesis pass · year-by-year structured walk · 11 steps
  1. 1996 High

    Established that ZnT2 confers zinc tolerance not by exporting zinc from the cell but by sequestering it into acidic intracellular vesicles, defining a distinct compartmentalization strategy versus the plasma-membrane exporter ZnT1.

    Evidence cDNA complementation of zinc-sensitive BHK cells with zinquin and acidic-compartment imaging plus fractionation

    PMID:8617223

    Open questions at the time
    • Transport stoichiometry and energetic driver not yet defined
    • Identity of the specific vesicular compartment (endosome vs lysosome) not resolved
  2. 2006 High

    Linked SLC30A2 to human disease by showing the H54R mutation mislocalizes ZnT2 to a perinuclear aggresome and reduces mammary zinc secretion, explaining transient neonatal zinc deficiency.

    Evidence Patient genomic sequencing, transfection/localization, mammary siRNA knockdown and zinc secretion assays

    PMID:17065149

    Open questions at the time
    • Whether aggresomal misfolding reflects a general folding defect or a specific targeting failure was not distinguished
    • Did not define the wild-type secretory trafficking route
  3. 2009 High

    Demonstrated that prolactin upregulates ZnT2 transcription via JAK2/STAT5 acting at defined promoter GAS sites, and that alternative splicing produces compartment-distinct isoforms, establishing layered control of where and how much ZnT2 is made.

    Evidence Luciferase reporters, ChIP, gel shift, dominant-negative STAT5, JAK2 inhibition; HA-isoform localization and transport assays

    PMID:19494234 PMID:19496757

    Open questions at the time
    • Functional significance of the plasma-membrane 35 kDa isoform not established
    • Did not connect transcriptional control to post-translational regulation
  4. 2010 High

    Extended ZnT2 function to additional secretory cell types and identified glucocorticoid/zinc-responsive promoter regulation, showing ZnT2 loads zinc into zymogen granules of pancreatic acini.

    Evidence Mouse dietary zinc manipulation, AR42J siRNA knockdown, promoter analysis, fluorescent zinc imaging; SNP localization studies in mammary cells

    PMID:20133611 PMID:20858712

    Open questions at the time
    • Mechanism by which naturally occurring SNPs cause organelle-specific mislocalization not defined
    • Physiological consequence of pancreatic ZnT2 loss in vivo not tested
  5. 2011 High

    Revealed a dual-organelle role by showing ZnT2 imports zinc into mitochondria via an N-terminal histidine-rich targeting motif, with consequences for ATP biogenesis and apoptosis, while vesicular sequestration protects against zinc cytotoxicity.

    Evidence GFP/HA fusions, truncation/point mutants, inner-membrane fractionation, mitochondrial zinc and ATP assays; breast tumor cell knockdown with ROS and lysosomal integrity readouts

    PMID:21289295 PMID:21353385

    Open questions at the time
    • How a single protein is partitioned between mitochondria and endolysosomes not resolved
    • Mitochondrial import mechanism across the inner membrane not biochemically reconstituted
  6. 2013 High

    Defined ZnT2 as an obligate dimer for function by showing transport- and dimerization-null (W152R), unstable (S296L), and dominant-negative dimer-forming (G87R) mutations underlie reduced milk zinc, linking oligomerization to activity and disease.

    Evidence Zinc-sensitive DT40/HC11/MCF-7 transport, dimerization, stability and co-IP assays with patient genetics

    PMID:22733820 PMID:23741301

    Open questions at the time
    • Structural basis of the dimer interface not empirically determined
    • Whether heterodimerization with other ZnT family members occurs not addressed
  7. 2014 High

    Showed prolactin also acts post-translationally, ubiquitinating ZnT2 at K4/K6 to transiently boost then degrade the transporter, providing a dynamic on/off control of zinc secretion.

    Evidence K4R/K6R mutagenesis, ubiquitination, vesicular zinc, secretion and degradation assays

    PMID:25016022

    Open questions at the time
    • Responsible E3 ligase not identified
    • Link between ubiquitination and trafficking versus degradation not fully separated
  8. 2015 High

    Connected ZnT2 trafficking to programmed mammary involution by showing TNFα-driven S296 dephosphorylation unmasks an L294L dileucine motif for AP-3-mediated lysosomal retargeting, loading lysosomal zinc to trigger lysosomal-mediated cell death, and that ZnT2-null mice fail normal mammary development.

    Evidence Phospho/dephospho-mimetic and L294V mutagenesis, AP-3 co-IP, in vivo adenoviral overexpression, lysosomal zinc and cathepsin B assays, ZnT2 knockout mouse phenotyping

    PMID:25620235 PMID:25808614 PMID:25851903

    Open questions at the time
    • Phosphatase/kinase controlling S296 not identified
    • How impaired STAT5 activation in knockouts mechanistically links to ZnT2 zinc transport not resolved
  9. 2018 Medium

    Broadened ZnT2 function beyond zinc storage to organelle homeostasis, showing it drives V-ATPase assembly and lysosome biogenesis/acidification, and that the common phosphorylation-prone T288S variant mislocalizes ZnT2 to ER/lysosomes causing stress and barrier defects.

    Evidence ZnT2 knockout mice and MEC knockdown with V-ATPase assembly and lysosome quantification; T288S phosphomimetic localization, ER stress, ROS, STAT3 and tight-junction assays

    PMID:29476070 PMID:29718697

    Open questions at the time
    • Molecular interaction by which ZnT2 promotes V-ATPase assembly not defined
    • T288S findings from a single lab
  10. 2019 Medium

    Defined the biophysical transport mechanism, establishing ZnT2 as an electroneutral 2H+/Zn2+ antiporter driven by the V-ATPase proton gradient and building alternating-access conformational models from bacterial YiiP homology.

    Evidence Transport assays with bafilomycin A1, Lyso-pHluorin pH measurement, TPEN chelation, multiscale computational modeling and confirmatory mutagenesis

    PMID:30388104 PMID:30893306

    Open questions at the time
    • No empirical high-resolution structure of human ZnT2
    • Stoichiometry inferred from pH and modeling rather than direct flux measurement
  11. 2022 Medium

    Extended ZnT2's physiological reach to innate immunity by showing it buffers cytoplasmic zinc to support TLR4/NF-κB signaling, autophagy and lysosome biogenesis in colonocytes, mast-cell granule zinc release driving GPR39/IL-6 wound healing, and Paneth-cell granule antimicrobial function.

    Evidence ZnT2 knockout mice and cell models with infection challenge, cytokine and autophagy assays; mast-cell knockout wound-healing with GPR39/IL-6-null epistasis; Paneth-cell granule and microbiota analyses

    PMID:28174721 PMID:31346193 PMID:36232769

    Open questions at the time
    • Direct molecular link between vesicular zinc and TLR4/NF-κB signaling not defined
    • Single-lab findings for each immune context

Open questions

Synthesis pass · forward-looking unresolved questions
  • How ZnT2 trafficking decisions integrate transcriptional, ubiquitination, and phosphorylation inputs to direct it among mitochondria, secretory granules and lysosomes in a cell-type-specific manner remains unresolved.
  • No empirical structure to map mutations and motifs onto conformational states
  • Enzymes controlling S296 phosphorylation and K4/K6 ubiquitination not identified
  • Mechanism partitioning ZnT2 between mitochondria and endolysosomes unknown

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0005215 transporter activity 4 GO:0140104 molecular carrier activity 2
Localization
GO:0005764 lysosome 5 GO:0005739 mitochondrion 2 GO:0005768 endosome 2 GO:0005783 endoplasmic reticulum 2 GO:0031410 cytoplasmic vesicle 2
Pathway
R-HSA-168256 Immune System 2 R-HSA-1852241 Organelle biogenesis and maintenance 2 R-HSA-382551 Transport of small molecules 2 R-HSA-5357801 Programmed Cell Death 2
Partners
AP3SLC30A2

Evidence

Reading pass · 23 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1996 ZnT2 (SLC30A2) confers resistance to zinc toxicity by facilitating vesicular sequestration of zinc into an acidic endosomal/lysosomal compartment. Unlike ZnT1 (plasma membrane), ZnT2 localizes to intracellular vesicles and accumulates zinc within them, as visualized by the zinc-specific fluorophore zinquin and the acidic compartment markers acridine orange and LysoTracker. cDNA complementation of zinc-sensitive BHK cells, zinquin fluorescence imaging, acridine orange/LysoTracker staining, subcellular fractionation The EMBO journal High 8617223
2006 A missense mutation H54R in SLC30A2/ZnT2 causes low milk zinc concentration and transient neonatal zinc deficiency. The H54R mutant protein accumulates in a perinuclear, aggresomal compartment rather than the normal secretory vesicle location, reducing zinc secretion from mammary epithelial cells. SLC30A2 gene knockdown in mammary epithelial cells also reduced zinc secretion. Genomic DNA sequencing, transient transfection in HEK-293 cells, siRNA knockdown in mammary epithelial cells, zinc secretion assays, co-expression experiments The Journal of biological chemistry High 17065149
2007 ZnT2 (SLC30A2) can independently of AP-3 function promote zinc accumulation in mature lysosomes. GFP-ZnT2 overexpression restored vesicular zinc storage capability in AP-3-deficient cells and elicited significant zinc accumulation in lysosomes that normally contained little chelatable zinc. siRNA-mediated AP-3 knockdown, GFP-ZnT2 overexpression, zinquin fluorescence imaging, human fibroblastoid cell line M1 Experimental cell research Medium 17349999
2009 Two distinct ZnT2 isoforms (~42 kDa and ~35 kDa) arise from alternative splicing of SLC30A2 and localize to distinct subcellular compartments: the 42 kDa isoform localizes primarily to the endosomal/secretory compartment and increases vesicular zinc, while the 35 kDa isoform associates with the plasma membrane. Both isoforms are functionally competent to transport zinc. Expression of HA-tagged ZnT2 isoforms in cells, immunofluorescence localization, zinc transport assays, Western blot The Biochemical journal Medium 19496757
2009 Prolactin transcriptionally upregulates ZnT2 expression in mammary epithelial cells through the JAK2/STAT5 signaling pathway. A proximal STAT5 binding site (GAS2: −377 to −368) in the ZnT2 promoter is critical for PRL-induced activation; a distal GAS1 site cooperates. Dominant-negative STAT5 abolished PRL-induced ZnT2 promoter activity. Luciferase reporter assay, JAK2 inhibitor (AG490) treatment, dominant-negative STAT5 construct, promoter mutagenesis, gel shift assay, chromatin immunoprecipitation American journal of physiology. Cell physiology High 19494234
2010 ZnT2 in pancreatic acinar cells localizes to zymogen granules and mediates zinc sequestration into them. ZnT2 expression is regulated by zinc via an MRE element and by the glucocorticoid/dexamethasone pathway requiring glucocorticoid receptor and STAT5 binding sites in the ZnT2 promoter. siRNA knockdown of ZnT2 increased cytoplasmic zinc and decreased zymogen granule zinc. Immunofluorescence localization, dietary zinc manipulation in mice, siRNA knockdown in AR42J cells, luciferase reporter/promoter analysis, fluorescent zinc measurement Proceedings of the National Academy of Sciences of the United States of America High 20133611
2010 Two naturally occurring SNPs in ZnT2 (L23P and R340C) cause distinct subcellular mislocalization and altered zinc metabolism: L23P (SNP1) mislocalizes to lysosomes causing lysosomal zinc accumulation and abrogated zinc secretion; R340C (SNP2) mislocalizes to Golgi, expands cytoplasmic zinc pools, elevates ROS, and increases zinc efflux. Expression of SNP-HA fusion proteins, immunofluorescence, FluoZin-3 fluorescence, ROS measurement, zinc secretion assay Physiological genomics Medium 20858712
2011 ZnT2 is associated with the inner mitochondrial membrane in mammary cells and functions as a zinc importer into mitochondria. A histidine-rich motif (51HHXH54) in the NH2 terminus is required for mitochondrial targeting of ZnT2. ZnT2-mediated expansion of mitochondrial zinc pools reduced ATP biogenesis and mitochondrial oxidation and increased apoptosis. Confocal microscopy of GFP/HA fusion proteins, truncated and point mutants, ZnT2-HA fractionation to inner mitochondrial membrane, siRNA knockdown, mitochondrial zinc uptake assays, ATP measurement American journal of physiology. Cell physiology High 21289295
2011 ZnT2 overexpression in MT-null malignant breast tumor cells (T47D) sequesters zinc into intracellular vesicles and protects cells from zinc cytotoxicity. Knockdown of ZnT2 increased cytoplasmic zinc pools, generated ROS, caused lysosomal swelling and cathepsin D leakage, and activated caspase-independent apoptosis. ZnT2 siRNA knockdown, 4X-MRE luciferase reporter, ROS measurement, lysosomal integrity assays (cathepsin D leakage), cell viability and tumor formation assays Cancer letters Medium 21353385
2012 The G87R mutation in ZnT2 causes ER-Golgi retention of the transporter and markedly impaired zinc transport. G87R exerts a dominant negative effect over wild-type ZnT2 by forming homodimers (established by co-immunoprecipitation), causing mislocalization and decreased stability of co-expressed WT ZnT2. Transient transfection in HC11 and MCF-7 cells, immunofluorescence, Western blot, vesicular zinc accumulation assay, zinc secretion assay, co-immunoprecipitation, 3D homology modeling The Journal of biological chemistry High 22733820
2013 The W152R mutation in ZnT2 abolishes both zinc transport activity and dimer complex formation, constituting a loss-of-function mutation. The S296L mutation retains zinc transport and dimerization but is extremely unstable. Compound heterozygosity (W152R/S296L) causes severe reduction (>90%) in milk zinc concentration. Functional zinc transport assay in zinc-sensitive DT40 cells, dimerization assay, cell-based stability assessment, genetic sequencing PloS one High 23741301
2014 Prolactin post-translationally stimulates ZnT2 ubiquitination at two N-terminal lysine residues (K4 and K6), which transiently augments vesicular zinc accumulation and zinc secretion from mammary epithelial cells, then promotes ZnT2 degradation to down-regulate zinc secretion. Mutagenesis of K4R and K6R inhibited ubiquitination, vesicular zinc accumulation, secretion, and protein degradation. Site-directed mutagenesis (K4R, K6R), ubiquitination assays, vesicular zinc accumulation assay, zinc secretion assay, Western blot for protein degradation The Journal of biological chemistry High 25016022
2015 ZnT2-mediated zinc transport into lysosomes and mitochondria is critical for lysosomal-mediated cell death (LCD) during mammary gland involution. Following weaning, ZnT2 abundance increases in lysosomes and mitochondria paralleling zinc accumulation. Adenoviral ZnT2 overexpression in vivo activated LCD and apoptosis; TNFα redistributes ZnT2 to lysosomes, increasing lysosomal zinc, causing lysosomal swelling, cathepsin B release, and LCD. Adenoviral ZnT2 expression in vivo, TNFα treatment of cultured MECs, immunofluorescence, lysosomal zinc measurement, cathepsin B release assay, apoptosis assays Scientific reports High 25620235
2015 ZnT2-null mice show impaired mammary gland expansion during development, defects in alveolar architecture, impaired STAT5 activation, unpolarized MECs, and reduced milk volume/composition during lactation, establishing ZnT2-mediated zinc transport as critical for mammary differentiation and function. ZnT2 knockout mouse model, histology, immunofluorescence, STAT5 activation assay, milk volume/composition analysis The Journal of biological chemistry High 25851903
2015 TNFα post-translationally retargets ZnT2 to lysosomes through dephosphorylation of S296 in the C-terminus, which uncovers a conserved dileucine motif (L294L) that enables AP-3 adaptor protein binding and trafficking of ZnT2 to lysosomes. Mutation of L294V eliminated TNFα-mediated lysosomal retargeting, lysosomal zinc accumulation, and LCD; phospho/dephospho-mimetics confirmed S296 dephosphorylation is required. Confocal microscopy, site-directed mutagenesis (L294V, phospho/dephospho-mimetics T281, T288, S296), co-immunoprecipitation (AP-3 binding), lysosomal zinc measurement, LCD assay Journal of cellular physiology High 25808614
2016 ZnT2 localizes to the membrane of Paneth cell secretory granules and is required for zinc import into these granules. Loss of ZnT2 in knockout mice causes spontaneous degranulation, hypodense granules with less active lysozyme, autophagosome accumulation, granule degradation, impaired bactericidal activity, and enrichment of specific gut microbiota (Bacteroidales S24-7). Immunofluorescence, sucrose gradient fractionation, electron microscopy, Zinpyr-1 fluorescent zinc imaging, ZnT2 knockout mice, 16S rRNA sequencing, lysozyme activity assay, bactericidal assay Cellular and molecular gastroenterology and hepatology High 28174721
2018 ZnT2 is a novel regulator of vacuolar ATPase (V-ATPase) assembly on lysosomes, driving lysosome biogenesis and acidification during mammary gland involution. Loss of ZnT2 in null mice inhibits V-ATPase assembly on lysosomes, decreasing lysosome abundance and size, and impairs alveolar regression and STAT3 phosphorylation during involution. TNFα promotes lysosome biogenesis and acidification via ZnT2, not through cytoplasmic zinc accumulation. ZnT2 knockout mice, immunofluorescence, V-ATPase assembly assays on lysosomes, lysosome abundance/size quantification, siRNA knockdown in cultured MECs, TNFα treatment, STAT3 phosphorylation assay American journal of physiology. Regulatory, integrative and comparative physiology High 29718697
2018 A common ZnT2 variant T288S causes hyperphosphorylation that retains ZnT2 in the ER and lysosomes, increasing ER and lysosomal zinc accumulation, ER stress, ROS generation, and STAT3 activation, leading to decreased zona occludens-1 abundance and increased tight junction permeability in mammary epithelial cells. Expression of T288S variant and phosphomimetics in vitro, immunofluorescence localization, ER/lysosomal zinc measurement, ER stress markers (breast milk and in vitro), ROS assay, STAT3 assay, tight junction permeability assay Scientific reports Medium 29476070
2019 ZnT2 is a proton-coupled zinc antiporter with an apparent stoichiometry of 2H+/Zn2+ ions, functioning as an electroneutral vesicular zinc exchanger driven by the proton motive force. V-ATPase inhibition by bafilomycin A1 abolished ZnT2-dependent vesicular zinc transport, and ZnT2 overexpression plus exogenous zinc caused vesicular pH alkalization (reversed by TPEN zinc chelation), consistent with proton-zinc antiport. Functional zinc transport assays, bafilomycin A1 treatment (V-ATPase inhibition), LysoTracker Red and Lyso-pHluorin pH measurement, TPEN zinc chelation, computational energy calculations PLoS computational biology Medium 30893306
2018 Computational modeling identified key residues in the ZnT2 permeation pathway consistent with alternating access mechanism; site-directed mutagenesis of these residues confirmed their functional role in zinc transport. Models of inward- and outward-facing ZnT2 conformations were constructed based on homology to bacterial YiiP. Multiscale computational modeling (coarse-grained Monte Carlo), homology modeling on YiiP crystal structure, site-directed mutagenesis, functional zinc transport assay PLoS computational biology Medium 30388104
2019 ZnT2 is required for zinc release from mast cell granules, and zinc released from mast cells signals through GPR39 to induce IL-6 production from skin fibroblasts, promoting wound healing. Wound healing was impaired in mice lacking IL-6 or GPR39. ZnT2 knockout mast cells, wound healing assay in mice, cytokine (IL-6) measurement, GPR39-null mice, IL-6-null mice Scientific reports Medium 31346193
2020 The T288S variant in ZnT2 promotes preferential phosphorylation, driving lysosomal localization, increased lysosome biogenesis and acidification, and significantly reduced cellular ATP levels in mammary epithelial cells. This variant was found in 20% of women producing low milk volume. Phosphomimetic constructs, immunofluorescence localization, lysosome biogenesis/acidification assays, ATP measurement, patient cohort stratification American journal of physiology. Cell physiology Medium 32320289
2022 ZnT2 in colonocytes transports zinc into vesicles, buffering cytoplasmic zinc pools required for TLR4 expression, NF-κB translocation, and cytokine expression in response to pathogens. ZnT2 is also critical for lysosome biogenesis and bacteria-induced autophagy in colonocytes. ZnT2 deletion in mice impaired the colonic response to Citrobacter rodentium infection. ZnT2 knockout mice, HT29 colonocyte culture, TLR4 expression assays, NF-κB translocation assay, cytokine measurement, lysosome biogenesis assay, autophagy assay, in vivo infection model International journal of molecular sciences Medium 36232769

Source papers

Stage 0 corpus · 38 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
1996 ZnT-2, a mammalian protein that confers resistance to zinc by facilitating vesicular sequestration. The EMBO journal 369 8617223
2006 Identification of a mutation in SLC30A2 (ZnT-2) in women with low milk zinc concentration that results in transient neonatal zinc deficiency. The Journal of biological chemistry 203 17065149
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 of the United States of America 100 20133611
2009 Zinc transporter-2 (ZnT2) variants are localized to distinct subcellular compartments and functionally transport zinc. The Biochemical journal 86 19496757
2012 A dominant negative heterozygous G87R mutation in the zinc transporter, ZnT-2 (SLC30A2), results in transient neonatal zinc deficiency. The Journal of biological chemistry 74 22733820
2013 Compound heterozygous mutations in SLC30A2/ZnT2 results in low milk zinc concentrations: a novel mechanism for zinc deficiency in a breast-fed infant. PloS one 73 23741301
2007 Zinc transporter 2 (SLC30A2) can suppress the vesicular zinc defect of adaptor protein 3-depleted fibroblasts by promoting zinc accumulation in lysosomes. Experimental cell research 61 17349999
2015 Essential Role for Zinc Transporter 2 (ZnT2)-mediated Zinc Transport in Mammary Gland Development and Function during Lactation. The Journal of biological chemistry 60 25851903
2016 ZnT2-Mediated Zinc Import Into Paneth Cell Granules Is Necessary for Coordinated Secretion and Paneth Cell Function in Mice. Cellular and molecular gastroenterology and hepatology 58 28174721
2011 ZnT2-overexpression represses the cytotoxic effects of zinc hyper-accumulation in malignant metallothionein-null T47D breast tumor cells. Cancer letters 54 21353385
2011 A histidine-rich motif mediates mitochondrial localization of ZnT2 to modulate mitochondrial function. American journal of physiology. Cell physiology 53 21289295
2009 Prolactin regulates ZNT2 expression through the JAK2/STAT5 signaling pathway in mammary cells. American journal of physiology. Cell physiology 48 19494234
2019 Mast cells play role in wound healing through the ZnT2/GPR39/IL-6 axis. Scientific reports 41 31346193
2015 ZnT2 is a critical mediator of lysosomal-mediated cell death during early mammary gland involution. Scientific reports 41 25620235
2017 The role of the zinc transporter SLC30A2/ZnT2 in transient neonatal zinc deficiency. Metallomics : integrated biometal science 38 28665435
2010 Functional analysis of two single nucleotide polymorphisms in SLC30A2 (ZnT2): implications for mammary gland function and breast disease in women. Physiological genomics 37 20858712
2013 Transient Neonatal Zinc Deficiency Caused by a Heterozygous G87R Mutation in the Zinc Transporter ZnT-2 (SLC30A2) Gene in the Mother Highlighting the Importance of Zn (2+) for Normal Growth and Development. International journal of endocrinology 36 24194756
2016 Novel mutations in SLC30A2 involved in the pathogenesis of transient neonatal zinc deficiency. Pediatric research 34 27304099
2019 ZnT2 is an electroneutral proton-coupled vesicular antiporter displaying an apparent stoichiometry of two protons per zinc ion. PLoS computational biology 30 30893306
2015 Exome Sequencing of SLC30A2 Identifies Novel Loss- and Gain-of-Function Variants Associated with Breast Cell Dysfunction. Journal of mammary gland biology and neoplasia 26 26293594
2018 ZnT2 is critical for lysosome acidification and biogenesis during mammary gland involution. American journal of physiology. Regulatory, integrative and comparative physiology 25 29718697
2014 Transient neonatal zinc deficiency due to a new autosomal dominant mutation in gene SLC30A2 (ZnT-2). Pediatric dermatology 24 24456035
2015 TNFα Post-Translationally Targets ZnT2 to Accumulate Zinc in Lysosomes. Journal of cellular physiology 23 25808614
2013 Prolactin receptor attenuation induces zinc pool redistribution through ZnT2 and decreases invasion in MDA-MB-453 breast cancer cells. Experimental cell research 22 24333596
2019 Milk-derived miRNA profiles elucidate molecular pathways that underlie breast dysfunction in women with common genetic variants in SLC30A2. Scientific reports 19 31481661
2018 A genetic variant in SLC30A2 causes breast dysfunction during lactation by inducing ER stress, oxidative stress and epithelial barrier defects. Scientific reports 19 29476070
2012 Polymorphisms of SLC30A2 and selected perinatal factors associated with low milk zinc in Chinese breastfeeding women. Early human development 17 22364884
2014 Prolactin (PRL)-stimulated ubiquitination of ZnT2 mediates a transient increase in zinc secretion followed by ZnT2 degradation in mammary epithelial cells. The Journal of biological chemistry 16 25016022
2020 A common genetic variant in zinc transporter ZnT2 (Thr288Ser) is present in women with low milk volume and alters lysosome function and cell energetics. American journal of physiology. Cell physiology 13 32320289
2018 Demonstrating aspects of multiscale modeling by studying the permeation pathway of the human ZnT2 zinc transporter. PLoS computational biology 11 30388104
2017 Transient Neonatal Zinc Deficiency Caused by a Novel Mutation in the SLC30A2 Gene. Pediatric dermatology 10 28111782
2020 A novel homozygous mutation p.E88K in maternal SLC30A2 gene as a cause of transient neonatal zinc deficiency. Experimental dermatology 8 32278324
2022 ZnT2 Is Critical for TLR4-Mediated Cytokine Expression in Colonocytes and Modulates Mucosal Inflammation in Mice. International journal of molecular sciences 5 36232769
2024 SLC30A2-Mediated Zinc Metabolism Modulates Gastric Cancer Progression via the Wnt/β-Catenin Signaling Pathway. Frontiers in bioscience (Landmark edition) 4 39473403
2023 Novel SLC30A2 mutations in the pathogenesis of transient neonatal zinc deficiency. Pediatric investigation 4 36967740
2023 Think zinc: Transient nutritional deficiency related to novel maternal SLC30A2 mutation potentially precipitated by antenatal proton pump inhibitor exposure. Clinical case reports 2 37082517
2026 Transient Neonatal Zinc Deficiency due to Maternal Variants in SLC30A2: An Emerging and Atypical Candidate Gene for Maternal Carrier Screening. American journal of medical genetics. Part A 1 41866816
2019 Correction: Demonstrating aspects of multiscale modeling by studying the permeation pathway of the human ZnT2 zinc transporter. PLoS computational biology 0 31042699

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