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Yan, Dong; Aiba, Isamu; Chen, Helen H.W.; Kuo, Macus Tien
Journal of inorganic biochemistry, 08/2016, Letnik: 161Journal Article
The human high-affinity copper transporter 1 (hCtr1) transports both Cu(I) and cisplatin (cDDP). Because Cu deficiency is lethal yet Cu overload is poisonous, hCtr1 expression is transcriptionally upregulated in response to Cu deficiency but is downregulated under Cu replete conditions in controlling Cu homeostasis. The up- and down-regulation of hCtr1 is regulated by Specific protein 1 (Sp1), which itself is also correspondingly regulated under these Cu conditions. hCtr1 expression is also upregulated by cDDP via upregulation of Sp1. The underlying mechanisms of these regulations are unknown. Using gel-electrophoretic mobility shift assays, we demonstrated here that Sp1-DNA binding affinity is reduced under Cu replete conditions but increased under reduced Cu conditions. Similarly, Sp1-DNA binding affinity is increased by cDDP treatment. This in vitro system demonstrated, for the first time, that regulation of Sp1/hCtr1 expression by these agents is modulated by the stability of Sp1-DNA binding, the first step in the Sp1-mediated transcriptional regulation process. Proposed models depicting Specific protein 1 (Sp1)-mediated transcriptional regulation of Sp1 itself and the human high-affinity copper transporter 1 (hCtr1) expression by bathocuproine sulfonate (BCS, a copper chelator) and cisplatin (cDDP) A and by copper B. Display omitted •The human high-affinity copper transporter (hCtr1) transports both Cu and cisplatin.•hCtr1 is regulated by Cu availability and cisplatin via Specific protein 1 (Sp1) factor.•Cu(II) de-stabilizes Sp1-DNA binding.•Cu chelator and cisplatin increase Sp1-DNA binding.•Effects of Sp1-DNA binding by Cu(II)/cDDP mirror their effects on hCtr1/Sp1 expression.
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JCR | SNIP | JCR | SNIP | JCR | SNIP | JCR | SNIP |
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in: SICRIS
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