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National Centre for Food Quality and Risk Assessment, Section of Nutrition, Istituto Superiore di Sanità, Rome, Italy
Division of Endocrinology and Metabolism, Cedars-Sinai Medical Center, University of California, Los Angeles, CA, USA
Department of Experimental Medicine and Pathology, University ‘La Sapienza’, Rome, Italy
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National Centre for Food Quality and Risk Assessment, Section of Nutrition, Istituto Superiore di Sanità, Rome, Italy
Division of Endocrinology and Metabolism, Cedars-Sinai Medical Center, University of California, Los Angeles, CA, USA
Department of Experimental Medicine and Pathology, University ‘La Sapienza’, Rome, Italy
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National Centre for Food Quality and Risk Assessment, Section of Nutrition, Istituto Superiore di Sanità, Rome, Italy
Division of Endocrinology and Metabolism, Cedars-Sinai Medical Center, University of California, Los Angeles, CA, USA
Department of Experimental Medicine and Pathology, University ‘La Sapienza’, Rome, Italy
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National Centre for Food Quality and Risk Assessment, Section of Nutrition, Istituto Superiore di Sanità, Rome, Italy
Division of Endocrinology and Metabolism, Cedars-Sinai Medical Center, University of California, Los Angeles, CA, USA
Department of Experimental Medicine and Pathology, University ‘La Sapienza’, Rome, Italy
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National Centre for Food Quality and Risk Assessment, Section of Nutrition, Istituto Superiore di Sanità, Rome, Italy
Division of Endocrinology and Metabolism, Cedars-Sinai Medical Center, University of California, Los Angeles, CA, USA
Department of Experimental Medicine and Pathology, University ‘La Sapienza’, Rome, Italy
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National Centre for Food Quality and Risk Assessment, Section of Nutrition, Istituto Superiore di Sanità, Rome, Italy
Division of Endocrinology and Metabolism, Cedars-Sinai Medical Center, University of California, Los Angeles, CA, USA
Department of Experimental Medicine and Pathology, University ‘La Sapienza’, Rome, Italy
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National Centre for Food Quality and Risk Assessment, Section of Nutrition, Istituto Superiore di Sanità, Rome, Italy
Division of Endocrinology and Metabolism, Cedars-Sinai Medical Center, University of California, Los Angeles, CA, USA
Department of Experimental Medicine and Pathology, University ‘La Sapienza’, Rome, Italy
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National Centre for Food Quality and Risk Assessment, Section of Nutrition, Istituto Superiore di Sanità, Rome, Italy
Division of Endocrinology and Metabolism, Cedars-Sinai Medical Center, University of California, Los Angeles, CA, USA
Department of Experimental Medicine and Pathology, University ‘La Sapienza’, Rome, Italy
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National Centre for Food Quality and Risk Assessment, Section of Nutrition, Istituto Superiore di Sanità, Rome, Italy
Division of Endocrinology and Metabolism, Cedars-Sinai Medical Center, University of California, Los Angeles, CA, USA
Department of Experimental Medicine and Pathology, University ‘La Sapienza’, Rome, Italy
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National Centre for Food Quality and Risk Assessment, Section of Nutrition, Istituto Superiore di Sanità, Rome, Italy
Division of Endocrinology and Metabolism, Cedars-Sinai Medical Center, University of California, Los Angeles, CA, USA
Department of Experimental Medicine and Pathology, University ‘La Sapienza’, Rome, Italy
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). The process of islet cell regeneration leads, after an initial phase of cell replication, to the acquisition of a number of phenotypic features that are characteristic of differentiated insulin-producing cells ( Hardikar 2004 ). However, whether such a
Sanford Consortium for Regenerative Medicine, University of California San Diego, La Jolla, California, USA
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Sanford Consortium for Regenerative Medicine, University of California San Diego, La Jolla, California, USA
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Sanford Consortium for Regenerative Medicine, University of California San Diego, La Jolla, California, USA
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to the mesenchymal portions of the placenta, including the fetal vasculature, the TE differentiates into two major trophoblast subtypes: villous trophoblast (labyrinthine trophoblast in mouse), involved in gas and nutrient exchange, and extravillous
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Post-Graduation Program of Biotechnology, National Institute of Metrology, Quality and Technology – INMETRO, Rio de Janeiro, Brazil
Multidisciplinary Center for Biological Research (Numpex-Bio), Federal University of Rio de Janeiro – Campus of Duque de Caxias, Rio de Janeiro, Brazil
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Multidisciplinary Center for Biological Research (Numpex-Bio), Federal University of Rio de Janeiro – Campus of Duque de Caxias, Rio de Janeiro, Brazil
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National Center of Structural Biology and Bioimage – CENABIO, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil
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perigonadal region of female NB-RKO mice to differentiate under adipogenic stimuli in vitro . In addition, to further explore mechanisms, we tested the effect of blocking the NB-R, employing a pharmacology antagonist, on the ability of the committed
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Introduction The major transcription factor families involved as key regulators of adipocyte differentiation include the nuclear hormone receptor peroxisome proliferator activated receptor (PPAR) γ and the CCAAT
Key Laboratory of Swine Genetics and Breeding of Agricultural Ministry and Key Laboratory of Agricultural Animal Genetics, Hunan Institute of Animal and Veterinary Science, Department of Animal Nutrition and Feed Science, Breeding and Reproduction of Ministry of Education, College of Animal Science and Technology, Huazhong Agricultural University, Wuhan 430070, People's Republic of China
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lineage and terminal differentiation, and finally differentiate into mature adipocytes ( Lefterova & Lazar 2009 ). Adipose tissue development is a complex process involving a cascade of multiple adipogenic transcription factors C/EBPβ, C/EBPδ, ADD1/SREBP1c
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crosstalk between them: osteoblasts are involved in the regulation of osteoclast differentiation through the receptor activator of nuclear factor κB ligand (RANKL)–RANK pathway, essential for a satisfactory balance between bone deposition and bone resorption
Endokrinologikum Hamburg, Falkenried 88, 20251 Hamburg, Germany
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Endokrinologikum Hamburg, Falkenried 88, 20251 Hamburg, Germany
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postovulatory rise in progesterone levels controls differentiation of this tissue in preparation for an implanting embryo. In the absence of pregnancy, ovarian hormone levels fall and the endometrial epithelial cells regress. At least this is the scenario in
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Introduction Adipogenesis is a multistep process through which progenitor cells differentiate into functional adipocytes and involves a cascade of adipogenic transcription factors and genes that define the adipocyte phenotype ( Rosen 2005 ). In
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obesity-related disorders. However, introduction of nucleic acids and, consequently, the manipulation of genes in fully differentiated 3T3-L1 adipocytes are difficult to achieve. pSLIK plasmids, encoding a tetracycline-regulated transcriptional unit in a
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particular, the balance between cell acquisition and cell loss ( Fruhbeck 2008 ). The proliferation of preadipocytes and their differentiation into mature adipocytes, combined with the apoptosis of preadipocytes, all contribute to the development of obesity