Functional analysis of two Sp1/Sp3 binding sites in murine Nanog gene promoter
文献类型:期刊论文
作者 | Wu, DY; Yao, Z |
刊名 | CELL RESEARCH
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出版日期 | 2006 |
卷号 | 16期号:3页码:319-322 |
关键词 | Nanog promoter Sp1 Sp3 |
通讯作者 | Wu, DY (reprint author), Chinese Acad Sci, Shanghai Inst Biol Sci, Inst Biochem & Cell Biol, Lab Mol Cell Biol,Lab Stem Cell Biol, 320 Yue Yang Rd, Shanghai 200031, Peoples R China.,dywu@sibs.ac.cn |
英文摘要 | Nanog gene plays a key role in maintaining pluripotency of ES cells and early embryonic cells. A 5' flank sequence of the Nanog gene has been reported to be regulated differentially, and two regulatory elements within the Nanog promoter, namely Oct-4 and Sox-2 binding sites, have been identified to regulate the transcriptional activity of Nanog gene. In this report, we identified the role of two putative Sp1 binding sites located in the Nanog gene 5'-flanking region in regulation of murine Nanog gene transcription. Mutation studies showed that the two sites were essential for the Nanog promoter activity. Gel shift and supershift analysis showed that both sites specifically bind Sp1 and Sp3. Furthermore, overexpression of dominant-negative Sp1 or Sp3 mutants significantly inhibits Nanog promoter activity. These results suggest that the transcription factor Sp1 and Sp3 are important for Murine Nanog gene expression. |
学科主题 | Cell Biology |
类目[WOS] | Cell Biology |
关键词[WOS] | TRANSCRIPTION FACTORS ; CELLS ; SP3 ; PLURIPOTENCY ; EXPRESSION ; OCT-4 |
收录类别 | SCI |
语种 | 英语 |
WOS记录号 | WOS:000237689100009 |
版本 | 出版稿 |
源URL | [http://202.127.25.143/handle/331003/1691] ![]() |
专题 | 上海生化细胞研究所_上海生科院生化细胞研究所 |
推荐引用方式 GB/T 7714 | Wu, DY,Yao, Z. Functional analysis of two Sp1/Sp3 binding sites in murine Nanog gene promoter[J]. CELL RESEARCH,2006,16(3):319-322. |
APA | Wu, DY,&Yao, Z.(2006).Functional analysis of two Sp1/Sp3 binding sites in murine Nanog gene promoter.CELL RESEARCH,16(3),319-322. |
MLA | Wu, DY,et al."Functional analysis of two Sp1/Sp3 binding sites in murine Nanog gene promoter".CELL RESEARCH 16.3(2006):319-322. |
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