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| Content Provider | MDPI |
|---|---|
| Author | Yoon, Hyun-Kyoung An, Hyun-Kyu Ko, Min Kim, Kyoung-Sook Mun, Seo-Won Kim, Dong-Hyun Kim, Cheol Kim, Cheorl-Ho Choi, Young Lee, Young-Choon |
| Abstract | In this research, we firstly demonstrated that physcion, an anthraquinone derivative, specifically increased the expression of the human α2,8-sialyltransferase (hST8Sia VI) gene in SK-N-BE(2)-C human neuroblastoma cells. To establish the mechanism responsible for the up-regulation of hST8Sia VI gene expression in physcion-treated SK-N-BE(2)-C cells, the putative promoter region of the hST8Sia VI gene was functionally characterized. Promoter analysis with serially truncated fragments of the 5′-flanking region showed that the region between −320 and −240 is crucial for physcion-induced transcription of hST8Sia VI in SK-N-BE(2)-C cells. Putative binding sites for transcription factors Pax-5 and NF-Y are located at this region. The Pax-5 binding site at −262 to −256 was essential for the expression of the hST8Sia VI gene by physcion in SK-N-BE(2)-C cells. Moreover, the transcription of hST8Sia VI induced by physcion in SK-N-BE(2)-C cells was inhibited by extracellular signal-regulated protein kinase (ERK) inhibitor U0126 and p38 mitogen-activated protein kinase (MAPK) inhibitor SB203580, but not c-Jun N-terminal kinase (JNK) inhibitor SP600125. These results suggest that physcion upregulates hST8Sia VI gene expression via ERK and p38 MAPK pathways in SK-N-BE(2)-C cells. |
| File Size | 4465664 |
| File Format | |
| e-ISSN | 14220067 |
| DOI | 10.3390/ijms17081246 |
| Journal | International Journal of Molecular Sciences |
| Issue Number | 8 |
| Volume Number | 17 |
| Language | English |
| Publisher Date | 2016-08-02 |
| Access Restriction | Open |
| Subject Keyword | physcion hST8Sia VI SK-N-BE(2)-C transcription factor Pax-5 signal pathway |
| Content Type | Text |
| Resource Type | Article |
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