Ask about this productRelated genes to: SLC30A3 Blocking Peptide
- Gene:
- SLC30A3 NIH gene
- Name:
- solute carrier family 30 member 3
- Previous symbol:
- ZNT3
- Synonyms:
- -
- Chromosome:
- 2p23.3
- Locus Type:
- gene with protein product
- Date approved:
- 1997-12-12
- Date modifiied:
- 2016-02-17
Related products to: SLC30A3 Blocking Peptide
Related articles to: SLC30A3 Blocking Peptide
- Stroke is one of the leading causes of adult disability and death worldwide. Inflammation-induced microvascular dysfunction and increased blood-brain barrier (BBB) permeability are major contributors to cerebral ischemia/reperfusion (I/R) injury. Previous studies have shown that zinc accumulation in microvessels contributes to BBB disruption following I/R. However, the mechanisms linking zinc accumulation to microvascular inflammation remain poorly understood. - Source: PubMed
Guo ZhengranShi WenjuanChen XiaodongYuan ShuhuaJi XunmingQi Zhifeng - Microglia exhibit phenotypic plasticity between anti-inflammatory M2 and pro-inflammatory M1 states, and the transition from M2 to M1 is implicated in the progression of acute brain injuries. However, the molecular mechanisms that regulate this phenotypic shift remain poorly understood. Zn, stored in presynaptic vesicles, is extracellularly released during pathological events, such as cerebral ischemia, and modulates microglial function. In this study, we aimed to investigate the role of extracellular Zn in the M2-to-M1 transition using BV2 microglial cells. Pretreatment with ZnCl during M2 polarization significantly suppressed lipopolysaccharide-induced production of interleukin (IL)-6 and tumor necrosis factor-α following the phenotypic shift. Among the zinc transporters, Zrt- and Irt-related protein 12 (ZIP12) expression was markedly upregulated by IL-4 stimulation, and siRNA-mediated knockdown of ZIP12 abolished the Zn-mediated suppression of pro-inflammatory cytokine production. Furthermore, ZIP12 knockdown reduced intracellular Zn accumulation in IL-4-treated microglia, as revealed by FluoZin-3 fluorescence. These findings indicate that extracellular Zn is taken up via ZIP12 during M2 polarization and subsequently acts to suppress pro-inflammatory cytokine production, thereby restraining the shift toward an M1 phenotype. - Source: PubMed
Publication date: 2025/10/30
Aratake TakaakiHigashi YouichirouShimizu TakahiroFukata SatoshiSaito Motoaki - Alzheimer's disease (AD) is a progressive neurodegenerative disorder with unclear pathogenic mechanisms. Dysregulated zinc metabolism contributes to AD pathology. This study aimed to identify zinc metabolism-related hub genes to provide potential biomarkers and therapeutic targets for AD. - Source: PubMed
Publication date: 2025/11/13
Bai RuyuCheng ZhiyunDiao Yong - Zinc plays a critical role in memory, learning, and neuronal function, with dysregulation increasingly implicated in neurodegenerative diseases such as Alzheimer's disease (AD). This study aimed to investigate whether changes in the expression of zinc transporter proteins, ZnT3 and ZIP3, in the retina mirror those in the brain, and to explore their potential as non-invasive biomarkers for early AD detection. Immunofluorescence and Western blotting were used to assess ZnT3 and ZIP3 expression in the retina and hippocampus of APP/PS1 and WT mice (9 and 18 months), as well as in human post-mortem tissues (9 AD and 6 control cases). To further investigate the regulatory role of ZnT3 in zinc homeostasis and its influence on tissue zinc concentrations, we quantified zinc levels in retinal and hippocampal tissues from WT and ZnT3 knockout mice using inductively coupled plasma-mass spectrometry (ICP-MS). ZnT3 and ZIP3 levels were significantly higher in the retina and hippocampus of healthy controls compared to AD cases across both mouse and human samples. ICP-MS analysis confirmed significantly lower zinc concentrations in ZnT3 knockout mice compared to WT controls in both the These findings demonstrate that retinal ZnT3 and ZIP3 expression changes mirror those observed in the hippocampus during AD progression. This suggests their potential as retinal biomarkers for Alzheimer's disease. Notably, ZnT3 shows strong promise for early, non-invasive detection of AD. Further validation in larger cohorts is warranted. - Source: PubMed
Publication date: 2025/10/01
Mashkani Seyed Mostafa HosseinpourBishop DavidAdlard Paul AMojtaba Golzan S - Tumor-induced osteomalacia (TIO) is a rare disorder caused by a phosphaturic mesenchymal tumor (PMT) secreting fibroblast growth factor 23 (FGF23). The aim of this study was to analyze PMTs for their transcriptomic characteristics. We performed single-cell RNA (n = 3) alongside bulk RNA sequencing of PMTs (n = 5) and surrounding bone tissue (n = 4) obtained during tumor removal in 10 patients (age 44 (41;64), serum phosphate (Pi)- 0.54 (0.43; 0.59) mM/L, FGF23-113 (40; 205) pg/ml). We revealed a total of 22,449 cells divided into 13 different categories. We identified the heterogeneity of the PMT cell cluster and subsequently divided it into two tumor clusters 1 and 2 characterized by the deeper epithelial-mesenchymal phenotype transition, higher FGF23 expression as well as various SNP and CNV. We further identified tumor cell differentiation driving regulons ERG and EGR3, based on scoring by allele expression and velocity based pseudotime on a trajectory that may play a critical role in the tumorigenesis of PMTs. In both single-cell and bulk transcriptome analysis we found upregulation of vesicle-specific and exocytosis associated genes (SLC30A3, SYT1, STX1A and SNAP25) which most likely represent molecular mechanisms of active secretion in all PMT samples. We report transmembrane protein coding genes expressed in all PMTs specifically in tumor cell clusters (PHEX, ERBB4, PCDH7, LRRFIP2) which are suggested as potential diagnostic targets. We confirmed the presence of FN1-FGFR1 fusion genes and Klotho expression in most PMTs (6 out of 8). Conclusion: specific SNARE proteins gene upregulation along with transcriptional signatures of PMT offer new insights into its pathogenesis which may be further studied for diagnostic and therapeutic interventions. - Source: PubMed
Publication date: 2025/09/11
Gronskaia Sofia ADeviatiiarov Ruslan MChekhonin Vladimir PDedov Ivan IBuklemishev Yuriy VBoulytcheva Irena VUtkina Marina VPopov Sergei VRodionova Svetlana SRozhinskaya Liudmila YGusev Oleg ABelaya Zhanna E