发起人
塔塔盒子
响应元素
基因
分子生物学
转录因子
生物
CAAT箱
结合位点
上游激活序列
抄写(语言学)
基因表达
遗传学
语言学
哲学
作者
Tatsushi Yoshida,Toshiyuki Sakai
出处
期刊:Elsevier eBooks
[Elsevier]
日期:2004-01-01
卷期号:: 35-49
被引量:17
标识
DOI:10.1016/s0083-6729(04)67003-8
摘要
TRAIL-R2 promoter does not have a typical TATA-box but two functional Sp1-binding sites. TRAIL-R2 promoter belongs to the class of TATA-less and GC-box-containing promoters. The minimal promoter element is contained in the region spanning -198 to -116 upstream of translational initiation codon ATG. Computer analysis shows putative transcription factor binding sites such as c-Ets, AML-1a, c-Myb, Sp1, and GATA-1 in TRAIL-R2 promoter. Hypermethylation of TRAIL-R2 is not frequent compared with that of TRAIL-R3 and TRIAL-R4. There are no potential transcription factor binding sites in highly homologous regions between TRAIL-R2 promoter and TRAIL-R1 promoter, or between TRAIL-R2 promoter and mouse homologue mouse killer (MK) promoter. TRAIL-R2 is known to be a downstream gene of p53, a tumor-suppressor gene, and a p53-binding site in TRAIL-R2 intron 1 is responsible for p53-dependent transcription. Thapsigargin, endoplasmic reticulum Ca(2+)-ATPase inhibitor calcium releaser, upregulates TRAIL-R2 expression via the promoter region. Many regulators of TRAIL-R2 have been reported. However, it has not been demonstrated whether they regulate TRAIL-R2 via the promoter region. Here, we show a list of these regulators. Finally, we demonstrate the possibility of cancer therapy using regulation of TRAIL-R2 promoter.
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