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- W3172075876 abstract "We have shown that the extracellular chelator DTPA (diethylenetriaminepentaaceticacid) promotes efflux of Zn65 from prelabeled rat primary hepatocytes, but increases retention of label in H4IIE hepatoma cells. To further understand this difference between primary cells and the corresponding cancer cell line, we investigated the effects of immortalizing primary cells on their zinc homeostasis. Freshly isolated rat hepatocytes were electroporated with the SV40 large T-antigen-coding-plasmid, pSV3-neo. Successful transformation was demonstrated by continued growth in the presence of neomycin. When these cells were pre-labeled with Zn65, DTPA decreased efflux of Zn65, similarly to hepatoma cells and differently from primary hepatocytes. This homeostatic change may be required to account for the greater zinc requirements of rapidly dividing cells. To further understand the mechanism of DTPA inducedzinc retention we down-regulated the expression of the plasma membrane located zinc efflux transporter, ZnT-1, in rat hepatoma cells using vector-based shRNA interference. Expression of ZnT-1 protein was reduced to approximately 50%. Down-regulation of ZnT-1 resulted in greater retention of Zn65 in control cells. However, DTPA increased rather than decreased efflux of label from knockdown cells, suggesting that functional ZnT-1 is required for the decreased efflux seen with DTPA in normal cells. Grant Funding Source: UConn Research Foundation" @default.
- W3172075876 created "2021-06-22" @default.
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- W3172075876 date "2010-04-01" @default.
- W3172075876 modified "2023-10-16" @default.
- W3172075876 title "The Effects of Transformation and ZnT‐1 Silencing on Zinc Homeostasis in Cultured Cells" @default.
- W3172075876 doi "https://doi.org/10.1096/fasebj.24.1_supplement.718.1" @default.
- W3172075876 hasPublicationYear "2010" @default.
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