Disease relevance of Slc30a1

• ZnT-1 expression in astroglial cells protects against zinc toxicity and slows the accumulation of intracellular zinc [1].
• The induction of ZnT-1 mRNA in CA1 pyramidal neurons fated to die after transient ischemia is of interest to the study of postischemic events and the molecular mechanisms underlying delayed neuronal death [2].

High impact information on Slc30a1

• Zinc transporter (ZnT) 3 has been identified as a putative transporter of zinc into synaptic vesicles of neurons and is found in brain areas such as hippocampus and cortex [3].
• Four putative zinc transporters, known as ZnT-1 through ZnT-4, have now been described [4].
• Immunofluorescence demonstrated that intestinal ZnT-1 was most abundant at the basolateral surface of enterocytes lining the villi of the duodenum and jejunum [4].
• Zn2+ was shown to accumulate in CA1 pyramidal neurons expressing ZnT-1 mRNA after the ischemia by using zinquin, a zinc-specific fluorescent dye [2].
• Expression of zinc transporter gene, ZnT-1, is induced after transient forebrain ischemia in the gerbil [2].

Chemical compound and disease context of Slc30a1

• L-type Ca(2+) channel-mediated Zn(2+) toxicity and modulation by ZnT-1 in PC12 cells [5].

Biological context of Slc30a1

• Our findings therefore indicate that ZnT-1 modulates the permeation of cations through LTCC, thereby, regulating cation homeostasis through this pathway [6].
• Expression of ZnT-1, -2 and -4 changes markedly during gestation and lactation from highly abundant to undetectable [7].
• Upregulation of ZnT-1 and ZnT-2 by dietary zinc strongly implicates these transporters in zinc acquisition and/or storage for subsequent systemic needs [7].
• When zinc was provided as a single oral dose (70 mg/kg body), ZnT-1 and ZnT-2 mRNA levels were increased many fold in small intestine, liver and kidney, whereas ZnT-4 gene expression was not changed [8].

Anatomical context of Slc30a1

• Pretreatment with zinc induced a 4-fold increase in the expression of the putative zinc transporter ZnT-1 in astroglia as shown by immunoblot analysis [1].
• Immunohistochemical analysis demonstrated endogenous ZnT-1 expression in cultured astroglia, microglia, and oligodendrocytes [1].
• Expression of ZnT-1 and -2 is regulated by dietary zinc in many organs including small intestine and kidney [7].
• To test the hypothesis that the plasma membrane transporter, ZnT-1, modulates Zn(2+) neurotoxicity, we generated stable PC12 cell lines overexpressing wild type or dominant negative forms of rat ZnT-1 (rZnT-1) [5].
• Thus, DEHP might exert its toxic effects on the testis by altering the expression of ZnT-1 [9].

Associations of Slc30a1 with chemical compounds

• Rats fed a low Zn or low vitamin A diet had lower ZnT-1 protein and higher ZnT-4 mRNA expression and protein levels compared with controls [10].
• Our study aim was to investigate the effect of acute and chronic exposure to various glucose concentrations on zinc in secretory vesicles, the relation between zinc and insulin, and the presence of two zinc transporters, ZnT1 and ZnT4, in INS-1E cells [11].

Other interactions of Slc30a1

• Plasma and brain Zn concentrations were measured, brain Zn uptake was assessed using (65)Zn, brain metallothionein-I and -III; LIV-1, zinc transporter ZnT-1, and ZnT-3 expression was measured by semiquantitative RT-PCR [12].
• ZnT-1 and ZnT-2 mRNAs were markedly greater in both tissues when a supplemental zinc intake (180 mg Zn/kg) was provided [8].
• Zinc content in testes was determined by atomic absorption spectrophotometry, and ZnT-1 mRNA was quantified by the branched DNA signal amplification method [9].

Analytical, diagnostic and therapeutic context of Slc30a1

• By Western blot analysis, intestinal and liver ZnT-1 protein migrated as a 42- and 36-kDa protein, respectively [4].
• These results represent studies on the expression of intestinal and hepatic ZnT-1 in an intact animal model [4].

References