Cell cycle-dependent regulation of TIAP/m-survivin expression

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• 作者：Otaki ; Masayuki ; Hatano ; Masahiko ; Kobayashi ; Koichi ; Ogasawara ; Takeshi ; Kuriyama ; Takayuki ; et. al.
• 关键词：TIAP/m-survivin ; Promoter ; CDE/CHR ; Cell cycle ; Inhibitor of apoptosis ; G2/M ; BIR ; baculovirus IAP repeat ; CDE ; cell cycle-dependent elements ; CHR ; cell cycle gene homology region ; IAP ; inhibitor of apoptosis ; Luc ; the firefly luciferase gene ; PCR ; polyme
• 刊名：Biochimica et Biophysica Acta (BBA)/Gene Structure and Expression
• 出版年：2000
• 出版时间：September 7, 2000
• 年：2000
• 卷：1493
• 期：1-2
• 页码：188-194
• 全文大小：410 K

文摘

TIAP, a murine homologue of human survivin, is a member of the inhibitor of apoptosis (IAP) family and is specifically expressed at G2/M phase of the cell cycle. To elucidate regulatory mechanisms of the cycle-dependent expression, we have analyzed the promoter region of TIAP/mouse survivin (m-survivin). The 5′-flanking region of the TIAP/m-survivin gene contained a TATA-less promoter, two AP2 sites, three NF-kB sites, one Sp1 site, many cell cycle-dependent elements (CDEs) and one cell cycle gene homology region (CHR). Primer extension and 5′-rapid amplification of cDNA ends identified one transcription start site at position −100 upstream of the ATG start site (+1). TIAP/m-survivin promoter–luciferase analysis identified a minimal promoter region within the most proximal −271 bp upstream of the ATG start site, and the region between −410 and −272 was critical for the enhancer activity. The combination between the CHR at −51 and the CDE at −57 is also essential for the cell cycle-dependent expression. Mutation of the CDE/CHR element and the enhancer elements may cause disordered expression of TIAP/m-survivin to affect cell survival and oncogenesis.