scholarly journals The role of zinc transporter proteins as predictive and prognostic biomarkers of hepatocellular cancer

PeerJ ◽  
2021 ◽  
Vol 9 ◽  
pp. e12314
Author(s):  
Ceylan V. Bitirim
Keyword(s):  
Tumor Progression ◽  
Zinc Deficiency ◽  
Zinc Level ◽  
Zinc Transporter ◽  
Tumor Formation ◽  
Zinc Homeostasis ◽  
Zinc Transporters ◽  
Transporter Proteins ◽  
Grade Ii ◽  
Cellular Zinc

Identification of the key processes involved in the tumor progression, malignancy and the molecular factors which are responsible for the transition of the cirrhotic cells to the tumor cells, contribute to the detection of biomarkers for diagnosis of hepatocellular carcinoma (HCC) at an early stage. According to clinical data, HCC is mostly characterized by a significant decrease in zinc levels. It is strongly implied that zinc deficiency is the major event required in the early stages of tumor formation and development of malignancy. Due to this reason, the definition of the molecular players which have a role in zinc homeostasis and cellular zinc level could give us a clue about the transition state of the cirrhosis to hepatic tumor formation. Despite the well-known implications of zinc in the development of HCCthe correlation of the expression of zinc transporter proteins with tumor progression and malignancy remain largely unknown. In the present study, we evaluated in detail the relationship of zinc deficiency on the prognosis of early HCC patients. In this study, we aimed to test the potential zinc transporters which contribute tothe transformation of cirrhosis to HCCand the progression of HCC. Among the 24 zinc transporter proteins, the proteins to be examined were chosen by using Gene Expression Profiling Interactive Analysis (GEPIA) webpage and RNA-seq analysis using TCGA database. ZIP14 and ZIP5 transporters were found as common differentially expressed genes from both bioinformatic analyses. ZnT1, ZnT7 and ZIP7 transporters have been associated with tumor progression. Relative abundance of ZnT1, ZIP5 and ZIP14 protein level was determined by immunohistochemistry (IHC) in surgically resected liver specimens from 16 HCC patients at different stages. IHC staining intensity was analyzed by using ImageJ software and scored with the histological scoring (H-score) method. The staining of ZnT1 was significantly higher in Grade III comparing to Grade II and Grade I. On the contrary, ZIP14 staining decreased almost 10-foldcomparing to Grade Iand Grade II. ZIP5 staining was detected almost 2-fold higher in cirrhosis than HCC. But ZnT1 staining was observed almost 3-fold lower in cirrhosis comparing to HCC. Intracellular free zinc level was measured by flow cytometry in Hep40 and Snu398 cells using FluoZin-3 dye. The intracellular free zinc level was almost 9-fold decreased in poor differentiated Snu398 HCC cells comparing to well differentiated Hep40 HCC cells.This report establishes for the first time the correlation between the expression pattern of ZIP14, ZnT1 and ZIP5 and significant zinc deficiency which occurs concurrently with the advancing of malignancy. Our results provide new molecular insight into ZnT1, ZIP14 and ZIP5 mediated regulation of cellular zinc homeostasis and indicate that zinc transporters might be important factors and events in HCC malignancy, which can lead to the development of early biomarkers.

scholarly journals Zinc Transporter ZIP12 Maintains Zinc Homeostasis and Protects Spermatogonia From Oxidative Stress During Spermatogenesis

2021 ◽  
Author(s):  
Xinye Zhu ◽  
Chengxuan Yu ◽  
Wangshu Wu ◽  
Lei Shi ◽  
Chenyi Jiang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Viability ◽  
Male Fertility ◽  
Sperm Quality ◽  
Zinc Level ◽  
Zinc Transporter ◽  
Zinc Homeostasis ◽  
Mouse Testis ◽  
Zinc Transporters ◽  
Wide Range

Abstract Background: Overwhelming evidences now suggest oxidative stress is a major cause of sperm dysfunction and male infertility. Zinc is an important non-enzyme antioxidant with a wide range of biological functions and plays a significant role in preserving male fertility. Notably, zinc trafficking through the cellular and intracellular membrane is endorsed by precise families of zinc transporters, i.e. SLC39s/ZIPs and SLC30s/ZnTs. However, the expression and function of zinc transporters in the male germ cells were rarely reported. The aim of this study is to determine the crucial zinc transporter responsible for the maintenance of spermatogenesis.Methods: In the present study, we investigated the expression of all fourteen ZIP members in mouse testis and further analyzed the characteristic of ZIP12 expression in testis and spermatozoa by qRT-PCR, immunoblot and immunohistochemistry analyses. To explore the antioxidant role of ZIP12 in spermatogenesis, an obese mouse model fed with high-fat-diet was employed to confirm the correlation between ZIP12 expression level and sperm quality. Furthermore, ZIP12 expression in response to oxidative stress in a spermatogonia cell line, C18-4 cells, was determined and its function involved in regulating cell viability and apoptosis was investigated by RNAi experiment. Results: We initially found that ZIP12 expression in mouse testis was significantly high compared to other members of ZIPs and its mRNA and protein were intensively expressed in testis rather than the other tissues. Importantly, ZIP12 was intensively abundant in spermatogonia and spermatozoa, both in mice and humans. Moreover, ZIP12 expression in testis significantly decreased in obese mice, which associated with reduced sperm zinc content, excessive sperm ROS, poor sperm quality and male subfertility. Similarly, its expression in C18-4 cells significantly declined in response to oxidative stress. Additionally, reduced ZIP12 expression by RNAi associated with a decline in zinc level subsequently caused low cell viability and high cell apoptosis in C18-4 cells. Conclusions: The zinc transporter ZIP12 is intensively expressed in testis, especially in spermatogonia and spermatozoa. ZIP12 may play a key role in maintaining intracellular zinc level in spermatogonia and spermatozoa, by which it resists oxidative stress during spermatogenesis and therefore preserves male fertility.

scholarly journals Expression Analysis of Zinc Transporters in Nervous Tissue Cells Reveals Neuronal and Synaptic Localization of ZIP4

2021 ◽  
Vol 22 (9) ◽  
pp. 4511
Author(s):  
Chiara A. De Benedictis ◽  
Claudia Haffke ◽  
Simone Hagmeyer ◽  
Ann Katrin Sauer ◽  
Andreas M. Grabrucker
Keyword(s):  
Brain Function ◽  
Zinc Homeostasis ◽  
Zinc Transporters ◽  
Excitatory Synapses ◽  
Short Term ◽  
Synaptic Localization ◽  
Zinc Levels ◽  
Rat Astrocyte ◽  
Cellular Zinc ◽  
The Brain

In the last years, research has shown that zinc ions play an essential role in the physiology of brain function. Zinc acts as a potent neuromodulatory agent and signaling ions, regulating healthy brain development and the function of both neurons and glial cells. Therefore, the concentration of zinc within the brain and its cells is tightly controlled. Zinc transporters are key regulators of (extra-) cellular zinc levels, and deregulation of zinc homeostasis and zinc transporters has been associated with neurodegenerative and neuropsychiatric disorders. However, to date, the presence of specific family members and their subcellular localization within brain cells have not been investigated in detail. Here, we analyzed the expression of all zinc transporters (ZnTs) and Irt-like proteins (ZIPs) in the rat brain. We further used primary rat neurons and rat astrocyte cell lines to differentiate between the expression found in neurons or astrocytes or both. We identified ZIP4 expressed in astrocytes but significantly more so in neurons, a finding that has not been reported previously. In neurons, ZIP4 is localized to synapses and found in a complex with major postsynaptic scaffold proteins of excitatory synapses. Synaptic ZIP4 reacts to short-term fluctuations in local zinc levels. We conclude that ZIP4 may have a so-far undescribed functional role at excitatory postsynapses.

ID: 60: ZINC DEFICIENCY PRIMES THE LUNG FOR VENTILATOR INDUCED LUNG INJURY

2016 ◽  
Vol 64 (4) ◽  
pp. 973.1-973
Author(s):  
J Englert ◽  
F Boudreault ◽  
M Pinilla-Vera ◽  
C Isabelle ◽  
A Arciniegas ◽  
...  
Keyword(s):  
Mechanical Ventilation ◽  
Lung Injury ◽  
Zinc Deficiency ◽  
Zinc Homeostasis ◽  
Adaptive Responses ◽  
Ventilator Induced Lung Injury ◽  
Human Lung Cells ◽  
Zinc Levels ◽  
Cellular Zinc

Mechanical ventilation is a necessary intervention to support patients with lung injury and the acute respiratory distress syndrome (ARDS), but can also exacerbate injury through mechanical stress-activated signaling pathways. We show that stretch applied to cultured human lung cells, and to mouse lungs in vivo, induces robust expression of metallothionein, a potent anti-oxidant and cyto-protective molecule critical for cellular zinc homeostasis. Furthermore, genetic deficiency of murine metallothionein genes exacerbated lung injury caused by injurious mechanical ventilation, identifying an adaptive role for these genes in limiting lung injury. Stretch induction of metallothionein required zinc and the zinc binding transcription factor MTF-1. We further show that dietary zinc-deficiency in mice potentiates ventilator-induced lung injury, and that plasma zinc levels are significantly reduced in human patients with ARDS compared to healthy and non-ARDS ICU controls, as well as to other critically ill patients without ARDS. Taken together, our findings identify a novel adaptive response of the lung to stretch mediated by metallothionein and zinc. These results demonstrate that failure of stretch-adaptive responses play an important role in exacerbating ventilator-induced lung injury, and identify zinc and metallothionein as targets for developing lung-protective interventions in patients requiring mechanical ventilation.

scholarly journals Zinc and the Zinc Transporter SLC39A10/ZIP10 Are Required for Heme Synthesis in Developing Erythroid Progenitors

2021 ◽  
Vol 5 (Supplement_2) ◽  
pp. 1320-1320
Author(s):  
Juyoung Kim ◽  
Jaekwon Lee ◽  
Moon-Suhn Ryu
Keyword(s):  
In Vitro Study ◽  
Fold Increase ◽  
Zinc Transporter ◽  
The Body ◽  
Zinc Homeostasis ◽  
Mean Corpuscular Hemoglobin ◽  
Erythroid Progenitors ◽  
Heme Synthesis ◽  
Cellular Zinc

Abstract Objectives Zinc is an essential nutrient for diverse biological processes in the body. Cellular zinc homeostasis is established through differential expressions of the transmembrane zinc transporter proteins, ZnTs and ZIPs. The aims of the current studies were to elucidate the roles of cellular zinc in erythrocyte maturation, and to determine the zinc transporters essential to erythroid zinc homeostasis. Methods G1E-ER4 mouse cells were employed as an in vitro study model of terminal erythroid differentiation. A cell-impermeable zinc chelator, diethylenetriamine pentaacetate (DTPA), was used to limit extracellular zinc availability. For gene silencing, gene-specific siRNAs were introduced to cells via Nucleofection. Functional impacts of zinc and gene deficiency were assessed via ICP-MS-based metal quantitation, heme assays, and gene expression assays using RNA-seq, qPCR, and western analyses. Results G1E-ER4 cells featured a 1.7-fold increase in total cellular zinc contents after 48 h of differentiation. Restriction of zinc import by 50 µM of DTPA led to less red coloration and lower increases in mean corpuscular hemoglobin contents by development. The heme deficiency by DTPA was fully restored by the addition of equimolar zinc, and was not due to changes in cellular iron contents. Zinc-deficient G1E-ER4 cells differentiated with normal Alas2 and Hbb-b1 transcript responses, but less Alad and alpha-globin expressions. Among the 24 zinc transporter genes, Zip10 produced the most prominent response to zinc restriction in differentiating erythroid cells. ZIP10-deficient G1E-ER4 cells were less efficient than control cells in hemoglobin production under zinc restriction. ZIP10 deficiency alone had no effects on the molecular indices of red cell hemoglobinization. Conclusions Our studies characterize zinc as a nutrient essential to normal erythroid maturation and heme synthesis. Moreover, we have identified a compensatory role of ZIP10 for erythroid zinc homeostasis during zinc restriction. Thus, poor zinc status and ZIP10 mutations might serve as potential risk factors and thus new therapeutic targets for anemia and other erythrocyte-related disorders. Funding Sources Supported by CFANS Graduate Fellowship to JK, and the Allen Foundation, Inc. and USDA NIFA Hatch Funds to M-SR.

scholarly journals Function, Structure, and Transport Aspects of ZIP and ZnT Zinc Transporters in Immune Cells

2018 ◽  
Vol 2018 ◽  
pp. 1-9 ◽  
Author(s):  
Bum-Ho Bin ◽  
Juyeon Seo ◽  
Sung Tae Kim
Keyword(s):  
Immune Cells ◽  
Drug Targets ◽  
Therapeutic Potential ◽  
Family Members ◽  
Zinc Transporter ◽  
Zinc Homeostasis ◽  
Zinc Transporters ◽  
Function Structure ◽  
Rich Domain ◽  
Zip Family

Zinc is an important trace metal in immune systems, and zinc transporters are involved in many immune responses. Recent advances have revealed the structural and biochemical bases for zinc transport across the cell membrane, with clinical implications for the regulation of zinc homeostasis in immune cells like dendritic cells, T cells, B cells, and mast cells. In this review, we discuss the function, structure, and transport aspects of two major mammalian zinc transporter types, importers and exporters. First, Zrt-/Irt-like proteins (ZIPs) mediate the zinc influx from the extracellular or luminal side into the cytoplasm. There are 14 ZIP family members in humans. They form a homo- or heterodimer with 8 transmembrane domains and extra-/intracellular domains of various lengths. Several ZIP members show specific extracellular domains composed of two subdomains, a helix-rich domain and proline-alanine-leucine (PAL) motif-containing domain. Second, ZnT (zinc transporter) was initially identified in early studies of zinc biology; it mediates zinc efflux as a counterpart of ZIPs in zinc homeostasis. Ten family members have been identified. They show a unique architecture characterized by a Y-shaped conformation and a large cytoplasmic domain. A precise, comprehensive understanding of the structures and transport mechanisms of ZIP and ZnT in combination with mice experiments would provide promising drug targets as well as a basis for identifying other transporters with therapeutic potential.

scholarly journals Zinc Homeostasis in Bone: Zinc Transporters and Bone Diseases

2020 ◽  
Vol 21 (4) ◽  
pp. 1236 ◽  
Author(s):  
Tongling Huang ◽  
Guoyong Yan ◽  
Min Guan
Keyword(s):  
Cell Types ◽  
Bone Diseases ◽  
Zinc Transporter ◽  
Zinc Homeostasis ◽  
Zinc Transporters ◽  
Bone Homeostasis ◽  
Microstructural Stability ◽  
Physiological Processes ◽  
Zip Family ◽  
Intracellular Compartments

Zinc is an essential micronutrient that plays critical roles in numerous physiological processes, including bone homeostasis. The majority of zinc in the human body is stored in bone. Zinc is not only a component of bone but also an essential cofactor of many proteins involved in microstructural stability and bone remodeling. There are two types of membrane zinc transporter proteins identified in mammals: the Zrt- and Irt-like protein (ZIP) family and the zinc transporter (ZnT) family. They regulate the influx and efflux of zinc, accounting for the transport of zinc through cellular and intracellular membranes to maintain zinc homeostasis in the cytoplasm and in intracellular compartments, respectively. Abnormal function of certain zinc transporters is associated with an imbalance of bone homeostasis, which may contribute to human bone diseases. Here, we summarize the regulatory roles of zinc transporters in different cell types and the mechanisms underlying related pathological changes involved in bone diseases. We also present perspectives for further studies on bone homeostasis-regulating zinc transporters.

scholarly journals Endoplasmic Reticulum Stress/Ca2+-Calmodulin-Dependent Protein Kinase/Signal Transducer and Activator of Transcription 3 Pathway Plays a Role in the Regulation of Cellular Zinc Deficiency in Myocardial Ischemia/Reperfusion Injury

2022 ◽  
Vol 12 ◽  
Author(s):  
Huanhuan Zhao ◽  
Dan Liu ◽  
Qiumei Yan ◽  
Xiyun Bian ◽  
Jing Yu ◽  
...  
Keyword(s):  
Er Stress ◽  
Zinc Deficiency ◽  
Calcium Concentration ◽  
Ischemia Reperfusion ◽  
Zinc Homeostasis ◽  
Dependent Protein Kinase ◽  
Stat3 Phosphorylation ◽  
Dependent Protein ◽  
Myocardial Ischemia Reperfusion ◽  
Cellular Zinc

Zinc homeostasis has been known to play a role in myocardial ischemia/reperfusion (I/R) injury, but the precise molecular mechanisms regulating the expression of ZIP transporters during reperfusion are still unclear. The aim of this study was to determine whether ER Stress/CaMKII/STAT3 pathway plays a role in the regulation of cellular zinc homeostasis. Zinc deficiency increased mRNA and protein expressions of the ER stress relevant markers Chop and Bip, and STAT3 phosphorylation in H9c2 or HL-1 cells, an effect that was abolished by ZnCl2. ER calcium concentration [(Ca2+)ER] was decreased and cytosolic calcium concentration [(Ca2+)I] was increased at the condition of normoxia or ischemia/reperfusion, indicating that zinc deficiency triggers ER stress and Ca2+ leak. Further studies showed that upregulation of STAT3 phosphorylation was reversed by Ca2+ chelator, indicating that intracellular Ca2+ is important for zinc deficiency-induced STAT3 activation. In support, zinc deficiency enhanced ryanodine receptors (RyR), a channel in the ER that mediate Ca2+ release, and Ca2+-calmodulin-dependent protein kinase (CaMKII) phosphorylation, implying that zinc deficiency provoked Ca2+ leak from ER via RyR and p-CaMKII is involved in STAT3 activation. Moreover, inhibition of STAT3 activation blocked zinc deficiency induced ZIP9 expression, and resulted in increased Zn2+ loss in cardiomyocytes, further confirming that STAT3 activation during reperfusion promotes the expression of ZIP9 zinc transporter to correct the imbalance in zinc homeostasis. In addition, suppressed STAT3 activation aggravated reperfusion injury. These data suggest that the ER Stress/CaMKII/STAT3 axis may be an endogenous protective mechanism, which increases the resistance of the heart to I/R.

scholarly journals The Effects of Short-Term Zinc Feeding on Zinc Absorption and Zinc Transporter Expression in the Small Intestine of Mice

2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 1827-1827
Author(s):  
Cassandra Olson ◽  
Alyssa Kelley ◽  
James McClung ◽  
Stephen Hennigar
Keyword(s):  
Small Intestine ◽  
Zinc Transporter ◽  
Zinc Homeostasis ◽  
Zinc Transporters ◽  
Zinc Absorption ◽  
Intestinal Segment ◽  
Deficient Diet ◽  
Us Government ◽  
Zinc Deficient Diet ◽  
Transporter Expression

Abstract Objectives Zinc homeostasis is primarily maintained by zinc transporters that regulate zinc uptake and efflux in the small intestine; however, no study to date has comprehensively examined zinc transporter expression in the small intestine of mice fed varying levels of dietary zinc. The objective of this study was to determine the effects of zinc absorption and zinc transporter expression in the small intestine of mice fed varying levels of zinc for one week. Methods Seven-week-old male C57BL/6 J mice were randomized to either a standard AIN-93 G diet containing 30 ppm zinc (zinc adequate) or modified AIN-93 G diets containing <1 ppm (zinc deficient) or 100 ppm zinc (zinc supplemented) for one week (n = 5–10/diet). Mice were given an oral gavage containing a slurry of zinc deficient feed and 10 μg 67 Zn; plasma isotope appearance was determined 6-h later by ICP-MS. Gene expression of Slc39a1–14 and Slc30a1–10 was determined in each intestinal segment (duodenum, jejunum, and ileum) by RT-qPCR. Results Plasma and liver zinc concentrations were not different after one week of feeding (P > 0.05 for both). Plasma appearance of 67 Zn was greater in mice fed the zinc deficient (mean ± SD: 0.36 ± 0.03 ng/mL) compared to the zinc adequate (0.22 ± 0.03 ng/mL) and zinc supplemented (0.22 ± 0.03 ng/mL, P < 0.0001 for both) diets. With the exception of Slc39a12, Slc30a3, and Slc30a8, the remaining zinc transporters were expressed across all diets and intestinal segments. Expression of Slc39a1, Slc39a4, Slc39a5, Slc39a7, Slc39a9, Slc39a11, Slc39a14, Slc30a2, Slc30a4, Slc30a5, Slc30a6, and Slc30a9 changed with diet (Pdiet < 0.05 for all); expression of Slc39a3, Slc39a7, Slc39a9 and Slc30a5 changed by intestinal segment (Psegment < 0.05 for all). Of those transporters expressed, Slc39a4 was positively associated with plasma appearance of 67 Zn (r = 0.645, P < 0.0001) and increased 7-fold in mice consuming the zinc deficient diet compared to the zinc adequate and zinc supplemented diets (P < 0.0001 for both). Conclusions Although most zinc transporters are expressed in the small intestine and likely function in concert, fluctuations in fractional zinc absorption are positively correlated with Slc39a4 expression in the small intestine. Funding Sources The views expressed herein are those of the authors and do not reflect official policy of the Army, DoD, or US Government. Supported by MRDC.

scholarly journals Regulation of ZIP and ZnT zinc transporters in zebrafish gill: zinc repression of ZIP10 transcription by an intronic MRE cluster

2008 ◽  
Vol 34 (2) ◽  
pp. 205-214 ◽  
Author(s):  
Dongling Zheng ◽  
Graham P. Feeney ◽  
Peter Kille ◽  
Christer Hogstrand
Keyword(s):  
Zinc Deficiency ◽  
Mrna Level ◽  
Negative Regulation ◽  
Zinc Homeostasis ◽  
Regulatory Control ◽  
Zinc Transporters ◽  
Alternative Promoters ◽  
Zinc Status ◽  
Zinc Availability ◽  
Excess Zinc

Resolving the mechanisms underlying the temporal and spatial profile of zinc transporter expression in response to zinc availability is key to understanding zinc homeostasis. The mRNA expression of seven zinc transporters was studied in zebrafish gills when treated with zinc deficiency/excess over a 14-day period. Of these, ZnT1, ZnT5, ZIP3, and ZIP10 were differentially expressed in response to changed zinc status. The mRNA level of zinc exporter, ZnT1, was upregulated in fish subjected to excess zinc and downregulated by zinc deprivation. This response was similar to that of metallothionein-2 (MT2). Zinc deficiency caused an increased abundance of mRNA for zinc importers ZnT5, ZIP3, and ZIP10. Expression of ZnT5 and ZIP10, but not ZIP3, was inhibited by excess zinc. Zinc influx function of ZIP10 was demonstrated by 65Zn transport assays in Xenopus oocyte expression experiments, suggesting that the inverse relationship between zinc availability and ZIP10 expression serves to maintain zinc homeostasis. Two distinct transcription start sites (TSS) for ZIP10 were found in gill and kidney. Luciferase assays and mutation/deletion analysis of DNA fragments proximal to the respective TSS revealed that ZIP10 has two alternative promoters (P1 and P2) displaying opposite regulatory control in response to zinc status. Positive as well as negative regulation by zinc involves MRE clusters in the respective promoters. These results provide experimental evidence for MREs functioning as repressor elements, implicating MTF1 involvement in the negative regulation of ZIP10. This is in contrast to the well-established positive regulation by MTF1 of other genes, such as MT2 and ZnT1.

The Physiological, Biochemical, and Molecular Roles of Zinc Transporters in Zinc Homeostasis and Metabolism

2015 ◽  
Vol 95 (3) ◽  
pp. 749-784 ◽  
Author(s):  
Taiho Kambe ◽  
Tokuji Tsuji ◽  
Ayako Hashimoto ◽  
Naoya Itsumura
Keyword(s):  
Zinc Transporter ◽  
Zinc Homeostasis ◽  
Zinc Transporters ◽  
Whole Body ◽  
Biological Processes ◽  
Transport Mechanisms ◽  
Intercellular Signaling ◽  
Zip Transporters ◽  
Related Proteins ◽  
Made In

Zinc is involved in a variety of biological processes, as a structural, catalytic, and intracellular and intercellular signaling component. Thus zinc homeostasis is tightly controlled at the whole body, tissue, cellular, and subcellular levels by a number of proteins, with zinc transporters being particularly important. In metazoan, two zinc transporter families, Zn transporters (ZnT) and Zrt-, Irt-related proteins (ZIP) function in zinc mobilization of influx, efflux, and compartmentalization/sequestration across biological membranes. During the last two decades, significant progress has been made in understanding the molecular properties, expression, regulation, and cellular and physiological roles of ZnT and ZIP transporters, which underpin the multifarious functions of zinc. Moreover, growing evidence indicates that malfunctioning zinc homeostasis due to zinc transporter dysfunction results in the onset and progression of a variety of diseases. This review summarizes current progress in our understanding of each ZnT and ZIP transporter from the perspective of zinc physiology and pathogenesis, discussing challenging issues in their structure and zinc transport mechanisms.

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