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Glycobiology Advance Access originally published online on February 15, 2006
Glycobiology 2006 16(5):375-389; doi:10.1093/glycob/cwj087
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© The Author 2006. Published by Oxford University Press. All rights reserved. For permissions, please e-mail: journals.permissions@oxfordjournals.org.
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Transcriptional regulation of the human GD3 synthase gene expression in Fas-induced Jurkat T cells: a critical role of transcription factor NF-{kappa}B in regulated expression

Young Kang1,2, Sung-Koo Kang1, Young-Choon Lee2, Hee-Jeong Choi1, Young-Seek Lee3, Soo-Young Cho3, Yong-Sam Kim4, Jeong-Heon Ko4, and Cheorl-Ho Kim1

1 Department of Biological Science, Sungkyunkwan University, Chunchun-Dong, Jangan-Gu, Suwon City, Kyunggi 440-746, Korea; 2 Faculty of Biotechnology, Dong-A University, Saha-Gu, Busan 604-714, Korea; 3 Division of Molecular and Life Science, Hanyang University, Ansan, Kyunggi-Do, Korea; and 4 Systematic Proteomic Research Center, Korea Research Institute of Bioscience and Biotechnology, Yusong-Gu, Daejon 305-600, Korea

1 To whom correspondence should be addressed; e-mail: chkimbio{at}skku.edu

Received on August 1, 2005; revised on December 27, 2005; accepted on February 3, 2006

The transcriptional regulation mechanisms involved in the up-regulation of Fas-induced GD3 synthase gene have not yet been elucidated. 5'-Rapid amplification of cDNA end (5'-RACE) using mRNA prepared from Fas-induced Jurkat T cells revealed the presence of multiple transcription start sites of human GD3 synthase gene, and the 5'-end analysis of the longest of its product showed that transcription started from 650 nucleotides upstream of the translational initiation site. Promoter analyses of the 5'-flanking region of the human GD3 synthase gene using luciferase gene reporter system showed strong promoter activity in Fas-induced Jurkat T cells. Deletion study revealed that the region from –1146 to –646 (A of the translational start ATG as position +1) was indispensable for the Fas response. This region lacks apparent TATA and CAAT boxes but contains putative binding sites for transcription factors c-Ets-1, cAMP-responsive element-binding (CREB) protein, activating protein 1 (AP-1), and NF-{kappa}B. Base-substitution experiment showed that only the NF-{kappa}B-binding site of putative binding sites is required for the maximal expression induced by Fas. Both DNase I footprint and electrophoretic mobility shift assays with the nuclear extract of Fas-induced Jurkat T cells revealed that NF-{kappa}B was bound specifically to the probe being mediated by its binding site in the promoter sequence. Taken together, these results indicate that NF-{kappa}B plays an essential role in the transcriptional activity of human GD3 synthase gene in Fas-induced Jurkat T cells. In addition, the translocation of NF-{kappa}B-binding protein to nucleus by Fas activation is also crucial for the increased expression of the GD3 synthase gene in Fas-activated Jurkat T cells.

Key words: Fas-induced Jurkat T cell / GD3 synthase / NF-{kappa}B / transcriptional regulation


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