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-producing cells in vitro . To achieve this, nuclear receptor subfamily 5, group A, member 1 ( NF5A1 that was previously known as SF-1 or AD4BP ) is a key molecule. NF5A1 is the steroidogenic tissue-specific transcription factor that controls the expression
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transcription factor mandatory for differentia tion of satellite cells into muscle fibers ( te Pas et al . 2000 ). Catabolic action of glucocorticoids The stimulatory effect of glucocorticoids on muscle proteolysis results from the activation of the major
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) and an adjacent CCAAT/enhancer-binding protein (C/EBP) site, and an activator protein-1 (AP-1) site; these elements can be bound by cognate transcription factors to regulate c- fos transcription in response to GH ( Meyer et al . 1993 , 1994
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) ( Garcia et al . 2014 ). Alternatively, as normal pituitary development depends on the sequential temporal and spatial expression of a cascade of signaling molecules and transcription factors, mutations in early ( HESX1, LHX3, LHX4, SOX3, OTX2 ) or late
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Hydrolase Exp Exp Exp Exp HIGD1A HIG1 hypoxia inducible domain family member 1A Scaffold/adaptor protein Exp Exp Exp Exp IRX2 Iroquois homeobox 2 Homeodomain transcription factor Exp Exp Exp Exp KCTD12
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transcriptional regulation by the hypoxia-inducible transcription factor, HIF-1 ( Grosfeld et al . 2001 , Ambrosini et al . 2002 ). The induction of leptin expression by hypoxia has also been reported in other cell types, including human trophoblast cell lines
Department of Endocrinology, Medical Research Institute, Tokyo Medical and Dental University, 1-5-45 Yushima Bunkyouku, Tokyo, Japan
Graduate School of Medicine, Tokyo Medical and Dental University, 1-5-45 Yushima Bunkyouku, Tokyo, Japan
Laboratory of Functional Genomics, Department of Medical Genome Science, Graduate School of Frontier Sciences, The University of Tokyo, 4-6-1 Shirokanedai, Minatoku, Tokyo, Japan
Division for Sex Differentiation, National Institute for Basic Biology, National Institutes of Natural Sciences, Higashiyama 5-1, Myondaiji-cho, Okazaki, Japan
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Department of Endocrinology, Medical Research Institute, Tokyo Medical and Dental University, 1-5-45 Yushima Bunkyouku, Tokyo, Japan
Graduate School of Medicine, Tokyo Medical and Dental University, 1-5-45 Yushima Bunkyouku, Tokyo, Japan
Laboratory of Functional Genomics, Department of Medical Genome Science, Graduate School of Frontier Sciences, The University of Tokyo, 4-6-1 Shirokanedai, Minatoku, Tokyo, Japan
Division for Sex Differentiation, National Institute for Basic Biology, National Institutes of Natural Sciences, Higashiyama 5-1, Myondaiji-cho, Okazaki, Japan
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Department of Endocrinology, Medical Research Institute, Tokyo Medical and Dental University, 1-5-45 Yushima Bunkyouku, Tokyo, Japan
Graduate School of Medicine, Tokyo Medical and Dental University, 1-5-45 Yushima Bunkyouku, Tokyo, Japan
Laboratory of Functional Genomics, Department of Medical Genome Science, Graduate School of Frontier Sciences, The University of Tokyo, 4-6-1 Shirokanedai, Minatoku, Tokyo, Japan
Division for Sex Differentiation, National Institute for Basic Biology, National Institutes of Natural Sciences, Higashiyama 5-1, Myondaiji-cho, Okazaki, Japan
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Department of Endocrinology, Medical Research Institute, Tokyo Medical and Dental University, 1-5-45 Yushima Bunkyouku, Tokyo, Japan
Graduate School of Medicine, Tokyo Medical and Dental University, 1-5-45 Yushima Bunkyouku, Tokyo, Japan
Laboratory of Functional Genomics, Department of Medical Genome Science, Graduate School of Frontier Sciences, The University of Tokyo, 4-6-1 Shirokanedai, Minatoku, Tokyo, Japan
Division for Sex Differentiation, National Institute for Basic Biology, National Institutes of Natural Sciences, Higashiyama 5-1, Myondaiji-cho, Okazaki, Japan
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Department of Endocrinology, Medical Research Institute, Tokyo Medical and Dental University, 1-5-45 Yushima Bunkyouku, Tokyo, Japan
Graduate School of Medicine, Tokyo Medical and Dental University, 1-5-45 Yushima Bunkyouku, Tokyo, Japan
Laboratory of Functional Genomics, Department of Medical Genome Science, Graduate School of Frontier Sciences, The University of Tokyo, 4-6-1 Shirokanedai, Minatoku, Tokyo, Japan
Division for Sex Differentiation, National Institute for Basic Biology, National Institutes of Natural Sciences, Higashiyama 5-1, Myondaiji-cho, Okazaki, Japan
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Department of Endocrinology, Medical Research Institute, Tokyo Medical and Dental University, 1-5-45 Yushima Bunkyouku, Tokyo, Japan
Graduate School of Medicine, Tokyo Medical and Dental University, 1-5-45 Yushima Bunkyouku, Tokyo, Japan
Laboratory of Functional Genomics, Department of Medical Genome Science, Graduate School of Frontier Sciences, The University of Tokyo, 4-6-1 Shirokanedai, Minatoku, Tokyo, Japan
Division for Sex Differentiation, National Institute for Basic Biology, National Institutes of Natural Sciences, Higashiyama 5-1, Myondaiji-cho, Okazaki, Japan
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Department of Endocrinology, Medical Research Institute, Tokyo Medical and Dental University, 1-5-45 Yushima Bunkyouku, Tokyo, Japan
Graduate School of Medicine, Tokyo Medical and Dental University, 1-5-45 Yushima Bunkyouku, Tokyo, Japan
Laboratory of Functional Genomics, Department of Medical Genome Science, Graduate School of Frontier Sciences, The University of Tokyo, 4-6-1 Shirokanedai, Minatoku, Tokyo, Japan
Division for Sex Differentiation, National Institute for Basic Biology, National Institutes of Natural Sciences, Higashiyama 5-1, Myondaiji-cho, Okazaki, Japan
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Department of Endocrinology, Medical Research Institute, Tokyo Medical and Dental University, 1-5-45 Yushima Bunkyouku, Tokyo, Japan
Graduate School of Medicine, Tokyo Medical and Dental University, 1-5-45 Yushima Bunkyouku, Tokyo, Japan
Laboratory of Functional Genomics, Department of Medical Genome Science, Graduate School of Frontier Sciences, The University of Tokyo, 4-6-1 Shirokanedai, Minatoku, Tokyo, Japan
Division for Sex Differentiation, National Institute for Basic Biology, National Institutes of Natural Sciences, Higashiyama 5-1, Myondaiji-cho, Okazaki, Japan
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Department of Endocrinology, Medical Research Institute, Tokyo Medical and Dental University, 1-5-45 Yushima Bunkyouku, Tokyo, Japan
Graduate School of Medicine, Tokyo Medical and Dental University, 1-5-45 Yushima Bunkyouku, Tokyo, Japan
Laboratory of Functional Genomics, Department of Medical Genome Science, Graduate School of Frontier Sciences, The University of Tokyo, 4-6-1 Shirokanedai, Minatoku, Tokyo, Japan
Division for Sex Differentiation, National Institute for Basic Biology, National Institutes of Natural Sciences, Higashiyama 5-1, Myondaiji-cho, Okazaki, Japan
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Department of Endocrinology, Medical Research Institute, Tokyo Medical and Dental University, 1-5-45 Yushima Bunkyouku, Tokyo, Japan
Graduate School of Medicine, Tokyo Medical and Dental University, 1-5-45 Yushima Bunkyouku, Tokyo, Japan
Laboratory of Functional Genomics, Department of Medical Genome Science, Graduate School of Frontier Sciences, The University of Tokyo, 4-6-1 Shirokanedai, Minatoku, Tokyo, Japan
Division for Sex Differentiation, National Institute for Basic Biology, National Institutes of Natural Sciences, Higashiyama 5-1, Myondaiji-cho, Okazaki, Japan
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, whereas GC lines lacking steroidogenesis completely lose the expression of this transcription factor ( Keren-Tal et al. 1997 ). These data account only for the role of Ad4BP in steroidogenesis and organogenesis, but it still remains unclear whether Ad4BP
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transcription factor E2F1 is involved in the regulation of cell cycle regulation ( Yoshikawa 2000 ). Additionally, the activity of cyclin–CDK complex can be regulated by the inhibitory interaction with CDK inhibitors (CKIs), such as p21 CIP1 , p27 KIP1 and p57
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Laboratory of Molecular and Cellular Biochemistry, Faculty of Dental Science, Kyushu University, Fukuoka, Japan
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Laboratory of Molecular and Cellular Biochemistry, Faculty of Dental Science, Kyushu University, Fukuoka, Japan
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.01 (Student’s t test). We previously showed that GluOC activates the transcription factor CREB (cAMP response element–binding protein) and increases the expression of the transcription factor FoxO1 (forkhead box protein O1) in 3T3-L1 adipocytes
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Introduction The transcription factor pleomorphic adenoma gene 1 (PLAG1) was first discovered via positional cloning when researchers were studying pleomorphic adenomas of the salivary glands ( Kas et al . 1997 ). Its role in various types of