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ZBSA – Freiburg Center for Systems Biology, University of Freiburg, Germany
Renal Division, University Hospital Freiburg, Germany
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ZBSA – Freiburg Center for Systems Biology, University of Freiburg, Germany
Renal Division, University Hospital Freiburg, Germany
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ZBSA – Freiburg Center for Systems Biology, University of Freiburg, Germany
Renal Division, University Hospital Freiburg, Germany
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negatively regulate the FOXO transcription factor DAF-16. Inhibition of the daf-2 receptor gene expression/activity or other genes in the insulin/IGF pathway can have three effects. (A) Early developmental downregulation, which affects many biological
Australian Centre for Blood Diseases, Eastern Clinical Research Unit, Department of Diabetes and Endocrinology, Biotechnology Division, Monash University, 6th Floor Burnett Tower, 89 Commercial Road, Prahran, Melbourne, Victoria, Australia 3181
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Australian Centre for Blood Diseases, Eastern Clinical Research Unit, Department of Diabetes and Endocrinology, Biotechnology Division, Monash University, 6th Floor Burnett Tower, 89 Commercial Road, Prahran, Melbourne, Victoria, Australia 3181
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Australian Centre for Blood Diseases, Eastern Clinical Research Unit, Department of Diabetes and Endocrinology, Biotechnology Division, Monash University, 6th Floor Burnett Tower, 89 Commercial Road, Prahran, Melbourne, Victoria, Australia 3181
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Australian Centre for Blood Diseases, Eastern Clinical Research Unit, Department of Diabetes and Endocrinology, Biotechnology Division, Monash University, 6th Floor Burnett Tower, 89 Commercial Road, Prahran, Melbourne, Victoria, Australia 3181
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promoter The human and mouse Nur77 promoters share highly conserved binding sites for NF-κB and AP-1 transcription factors ( Pei et al . 2005 ). To define the molecular mechanism of TZD-mediated inhibition of NUR77 expression, we performed EMSAs using
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, Meyerson et al. 1997 , Nakamura et al. 1997 ). It was recently reported that TERT protects neurons against Aβ- ( Zhu et al. 2000 ) or tropic factor withdrawal- and glutamate ( Fu et al. 2000 )-induced apoptosis. There is abundant evidence
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signalling pathways leading to the activation of transcription factors, with the NFκB pathway being of particular importance. The control of osteoclast differentiation and function by signalling pathways is highlighted by conditions in which key components of
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immunofluorescent staining was performed. There were two sets of co-expression pattern studies. First co-expression of nestin with transcription factors was examined. Co-staining of nestin with PDX-1 was observed at 15±4% in the monolayers after 2 months of culture
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mouse MSCs to increase the expression and secretion of VEGF ( Kinnaird et al . 2004 b , Wang et al . 2007 ). Hypoxia-inducible gene transcription is regulated by hypoxia-inducible factor-1 (HIF-1), which is essential for adaptive cellular responses to
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(PPARγ) have been identified as transcriptional factors ( MacDougald & Lane 1995 ) and are necessary for the transition of pre-adipocytes into adipocytes in vitro . In mammals, insulin growth factor-I (IGF-I) affects adipocyte proliferation and
Department of Clinical Biochemistry, University of Cambridge, Addenbrooke’s Hospital, Cambridge, UK
Steroid Research Unit, Center of Child and Adolescent Medicine, Justus-Liebig-University Giessen, Germany
Division of Endocrinology and Metabolism, Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan, USA
Medizinische Klinik - Innenstadt, Ludwig-Maximilians-University, Munich, Germany
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Department of Clinical Biochemistry, University of Cambridge, Addenbrooke’s Hospital, Cambridge, UK
Steroid Research Unit, Center of Child and Adolescent Medicine, Justus-Liebig-University Giessen, Germany
Division of Endocrinology and Metabolism, Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan, USA
Medizinische Klinik - Innenstadt, Ludwig-Maximilians-University, Munich, Germany
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Department of Clinical Biochemistry, University of Cambridge, Addenbrooke’s Hospital, Cambridge, UK
Steroid Research Unit, Center of Child and Adolescent Medicine, Justus-Liebig-University Giessen, Germany
Division of Endocrinology and Metabolism, Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan, USA
Medizinische Klinik - Innenstadt, Ludwig-Maximilians-University, Munich, Germany
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Department of Clinical Biochemistry, University of Cambridge, Addenbrooke’s Hospital, Cambridge, UK
Steroid Research Unit, Center of Child and Adolescent Medicine, Justus-Liebig-University Giessen, Germany
Division of Endocrinology and Metabolism, Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan, USA
Medizinische Klinik - Innenstadt, Ludwig-Maximilians-University, Munich, Germany
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Department of Clinical Biochemistry, University of Cambridge, Addenbrooke’s Hospital, Cambridge, UK
Steroid Research Unit, Center of Child and Adolescent Medicine, Justus-Liebig-University Giessen, Germany
Division of Endocrinology and Metabolism, Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan, USA
Medizinische Klinik - Innenstadt, Ludwig-Maximilians-University, Munich, Germany
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Department of Clinical Biochemistry, University of Cambridge, Addenbrooke’s Hospital, Cambridge, UK
Steroid Research Unit, Center of Child and Adolescent Medicine, Justus-Liebig-University Giessen, Germany
Division of Endocrinology and Metabolism, Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan, USA
Medizinische Klinik - Innenstadt, Ludwig-Maximilians-University, Munich, Germany
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Department of Clinical Biochemistry, University of Cambridge, Addenbrooke’s Hospital, Cambridge, UK
Steroid Research Unit, Center of Child and Adolescent Medicine, Justus-Liebig-University Giessen, Germany
Division of Endocrinology and Metabolism, Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan, USA
Medizinische Klinik - Innenstadt, Ludwig-Maximilians-University, Munich, Germany
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Department of Clinical Biochemistry, University of Cambridge, Addenbrooke’s Hospital, Cambridge, UK
Steroid Research Unit, Center of Child and Adolescent Medicine, Justus-Liebig-University Giessen, Germany
Division of Endocrinology and Metabolism, Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan, USA
Medizinische Klinik - Innenstadt, Ludwig-Maximilians-University, Munich, Germany
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Department of Clinical Biochemistry, University of Cambridge, Addenbrooke’s Hospital, Cambridge, UK
Steroid Research Unit, Center of Child and Adolescent Medicine, Justus-Liebig-University Giessen, Germany
Division of Endocrinology and Metabolism, Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan, USA
Medizinische Klinik - Innenstadt, Ludwig-Maximilians-University, Munich, Germany
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factors such as GATA-4 ( P = 0.0005), Wilms tumor gene-1 (WT-1; P < 0.0001), and steriodogenic factor-1 (SF-1; P = 0.0029) were significantly up-regulated after GDX, while other transcription factors such as FOG-1 ( P < 0.0001) and GATA-6 ( P = 0
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protein 7 (PAX7) denotes a myoblast that has not terminally differentiated and has the capacity to enter the cell cycle and proliferate ( Relaix et al . 2005 ). MRFs are a set of transcription factors, including MYF5 , MYOD , MYF6 and MYOG , that are
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Introduction Estrogen (E) control of cell proliferation is a complex process that is subject to regulation at many levels. The nuclear receptor/transcription factor estrogen receptor-α (ESR1) is the key regulatory participant, transducing E action