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15篇 您的检索式:作者名="Yatsuki"
    题名 作者 年代 出处 被引量
1Rctinoic acid receptor beta7, is epigenetically silenced either by DNA methylation or repressive histane modifications at the promoter in cervical cancer cells 显示文摘Zhang Z Job K Yatsuki H 2007Cancer Lett2007,247,2:1
2Effects of a peripheral cholinesterase inhibitor on cytokine production and autonomic nervous activity in a rat model of sepsis显示文摘Daisuke Setoguchi Henry Yatsuki Tomohito Sadahiro Masataka Nakamura Yo Hirayama Eizo Watanabe Yoshihisa Tateishi Shigeto Oda 2011Cytokine2011,,2:1
3Isolation of a novel gene from a human cell line with Pr-28 mAb which recognizes a nuclear antigen involved in the cell cycle显示文摘Matsuhashi S Yoshinaga H Yatsuki H 1997Res Comm Biochem Cell Mol Biol1997,1,1:1
4Retinoic acid receptor beta2 is epigenetically silenced either by DNA methylation or repressive histone modifications at the promoter in cervical cancer cells显示文摘Zhang Z Joh K Yatsuki H 2007Cancer Lett2007,247,2:1
5MeCP2 knockdown reveals DNA mcthylation-independent gene repression of target genes in living cells and a bias in the cellular location of target gene products 显示文摘Yakabe S Soejima H Yatsuki H 2008Genes Genet Syst2008,83,2:1
6Functional analysis of the p57kip2 gene mutation in Beckwith-Wiedemann syndrome显示文摘Zahurul A Bhuiyan Hitomi Yatsuki 1999Hum Genet1999,104,:1
7A novel human homologue of a DEAD -box RNA helicase family显示文摘Kitajima Y Yatsuki H Zhang R 1994Biochem Biophys Res Commun1994,54,8:1
8Functional analysis of the p57^kip2 gene mutation in Beckwith-Wiedemann syndrome 显示文摘Bhuiyan ZA Yatsuki H SaSaguri T 1999Hum Genet1999,104,:1
9Retinoic acid receptor (2 is epigenetically silenced either by DNA methylation or repressive histone modifications at the promoter in cervical cancer cells显示文摘Zhang Z M Joh K Yatsuki H 0,,2:1
10Retinoic acid receptor beta2 is epigenetically silenced either by DNA methylation or repressive histone modifications at the promoter in cervical cancer cells 显示文摘Zhang Z Joh K Yatsuki H 2007Cancer Lett2007,247,2:1
11Retinoic acid receptor beta2 is epi-genetical y silenced either by DNA methylation or repressive his-tone modifications at the promoter in cervical cancer cells显示文摘Zhang Z Joh K Yatsuki H 0,,02:1
12Carbon nanotubes on SiC powder surface grown by a vacuum heating process显示文摘Takikawa H Miyano R Yatsuki M 1998J Appl Phys1998,37,:1
13Retinoic acid receptor beta2 is epigenetically silenced either by DNA methylation or repressive histone modifications at the promoter in cervical cancer cells显示文摘Zhang Z Joh K Yatsuki H 0,,:1
14Retinoic acid receptor beta2 is epigenetically silenced either by DNA methylation or repressive histone modifications at the promoter in cervical cancer cells 显示文摘Zhang Z Joh K Yatsuki H 2007Cancer Lett2007,247,:1
15A developmental biological study of aldolase gene expression in Xenopus laevis显示文摘We cloned cDNAs for Xenopus aldolases A, B and C. These three aldolase genes are localized on different chromosomes as a single copy gene. In the adult, the aldolase A gene is expressed extensively in muscle tissues, whereas the aldolase B gene is expressed strongly in kidney, liver, stomach and intestine, while the aldolase C gene is expressed in brain, heart and ovary. In oocytes aldolase A and C mRNAs, but not aldolase B mRNA, are extensively transcribed. Thus, aldolase A and C mRNAs, but not B mRNA, occur abundantly in eggs as maternal mRNAs, and strong expression of aldolase B mRNA is seen only after the late neurula stage. We conclude that aldolase A and C mRNAs are major aldolase mRNAs in early stages of Xenopus embryogenesis which proceeds utilizing yolk as the only energy source, aldolase B mRNA, on the other hand, is expressed only later in development in tissues which are required for dietary fructose metabolism.We also isolated the Xenopus aldolase C genomic gene (ca. 12 kb) and found that its promoter (ca. 2 kb)contains regions necessary for tissue-specific expression and also a GC rich region which is essential for basal transcriptional activity.KOICHIRO SHIOKAWA, ERI KAJITA, HIROSHI HARA, HITOMI YATSUKI, KATSUJI HORI1 Laboratory of Molecular Embryology, Department of Biological Sciences, Graduate School of Science, TheUniversity of Tokyo, Hongo 7-3-1, Bunkyo ku, Tokyo 113-0033, Japan 2Medical Re 2002Cell Research2002,12,2:0
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