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Benoit Cox Department of Development and Regeneration, Cluster of Stem Cell and Developmental Biology, Unit of Stem Cell Research, University of Leuven (KU Leuven), Leuven, Belgium

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Heleen Roose Department of Development and Regeneration, Cluster of Stem Cell and Developmental Biology, Unit of Stem Cell Research, University of Leuven (KU Leuven), Leuven, Belgium

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Annelies Vennekens Department of Development and Regeneration, Cluster of Stem Cell and Developmental Biology, Unit of Stem Cell Research, University of Leuven (KU Leuven), Leuven, Belgium

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Hugo Vankelecom Department of Development and Regeneration, Cluster of Stem Cell and Developmental Biology, Unit of Stem Cell Research, University of Leuven (KU Leuven), Leuven, Belgium

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putative pituitary stem cell niche, encompassing the stem cells and the stem cell-supporting cells. The NOTCH (green), SHH (red), WNT (purple) and Hippo (blue) pathways are shown in their ‘off’ (left) and ‘on’ status (right). Interaction of the NOTCH

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Nicoleta C Olarescu Section of Specialized Endocrinology, Faculty of Medicine, Edison Biotechnology Institute, Heritage College of Osteopathic Medicine, Department of Endocrinology, Oslo University Hospital, Rikshospitalet, PO Box 4950, N‐0424 Oslo, Norway
Section of Specialized Endocrinology, Faculty of Medicine, Edison Biotechnology Institute, Heritage College of Osteopathic Medicine, Department of Endocrinology, Oslo University Hospital, Rikshospitalet, PO Box 4950, N‐0424 Oslo, Norway

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Darlene E Berryman Section of Specialized Endocrinology, Faculty of Medicine, Edison Biotechnology Institute, Heritage College of Osteopathic Medicine, Department of Endocrinology, Oslo University Hospital, Rikshospitalet, PO Box 4950, N‐0424 Oslo, Norway
Section of Specialized Endocrinology, Faculty of Medicine, Edison Biotechnology Institute, Heritage College of Osteopathic Medicine, Department of Endocrinology, Oslo University Hospital, Rikshospitalet, PO Box 4950, N‐0424 Oslo, Norway

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Lara A Householder Section of Specialized Endocrinology, Faculty of Medicine, Edison Biotechnology Institute, Heritage College of Osteopathic Medicine, Department of Endocrinology, Oslo University Hospital, Rikshospitalet, PO Box 4950, N‐0424 Oslo, Norway
Section of Specialized Endocrinology, Faculty of Medicine, Edison Biotechnology Institute, Heritage College of Osteopathic Medicine, Department of Endocrinology, Oslo University Hospital, Rikshospitalet, PO Box 4950, N‐0424 Oslo, Norway

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Ellen R Lubbers Section of Specialized Endocrinology, Faculty of Medicine, Edison Biotechnology Institute, Heritage College of Osteopathic Medicine, Department of Endocrinology, Oslo University Hospital, Rikshospitalet, PO Box 4950, N‐0424 Oslo, Norway

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Edward O List Section of Specialized Endocrinology, Faculty of Medicine, Edison Biotechnology Institute, Heritage College of Osteopathic Medicine, Department of Endocrinology, Oslo University Hospital, Rikshospitalet, PO Box 4950, N‐0424 Oslo, Norway

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Fabian Benencia Section of Specialized Endocrinology, Faculty of Medicine, Edison Biotechnology Institute, Heritage College of Osteopathic Medicine, Department of Endocrinology, Oslo University Hospital, Rikshospitalet, PO Box 4950, N‐0424 Oslo, Norway

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John J Kopchick Section of Specialized Endocrinology, Faculty of Medicine, Edison Biotechnology Institute, Heritage College of Osteopathic Medicine, Department of Endocrinology, Oslo University Hospital, Rikshospitalet, PO Box 4950, N‐0424 Oslo, Norway
Section of Specialized Endocrinology, Faculty of Medicine, Edison Biotechnology Institute, Heritage College of Osteopathic Medicine, Department of Endocrinology, Oslo University Hospital, Rikshospitalet, PO Box 4950, N‐0424 Oslo, Norway

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Jens Bollerslev Section of Specialized Endocrinology, Faculty of Medicine, Edison Biotechnology Institute, Heritage College of Osteopathic Medicine, Department of Endocrinology, Oslo University Hospital, Rikshospitalet, PO Box 4950, N‐0424 Oslo, Norway
Section of Specialized Endocrinology, Faculty of Medicine, Edison Biotechnology Institute, Heritage College of Osteopathic Medicine, Department of Endocrinology, Oslo University Hospital, Rikshospitalet, PO Box 4950, N‐0424 Oslo, Norway

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differentiation of MSCs are regulated in part by the Wnt/β-catenin signaling pathway. That is, activation of Wnt/β-catenin signaling decreases the adipogenic potential of MSCs ( Ross et al . 2000 , Lowe et al . 2011 ). Although MSCs have primarily been

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Mi-Hyun Kim
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Jae-Hwan Jee Division of Endocrinology and Metabolism, Division of Endocrinology and Metabolism, Samsung Biomedical Research Institute, 50 Ilwon-dong, Gangnam-gu, Seoul 135-710, Republic of Korea

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Sunyoung Park
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Myung-Shik Lee Division of Endocrinology and Metabolism, Division of Endocrinology and Metabolism, Samsung Biomedical Research Institute, 50 Ilwon-dong, Gangnam-gu, Seoul 135-710, Republic of Korea

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Kwang-Won Kim Division of Endocrinology and Metabolism, Division of Endocrinology and Metabolism, Samsung Biomedical Research Institute, 50 Ilwon-dong, Gangnam-gu, Seoul 135-710, Republic of Korea

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Moon-Kyu Lee Division of Endocrinology and Metabolism, Division of Endocrinology and Metabolism, Samsung Biomedical Research Institute, 50 Ilwon-dong, Gangnam-gu, Seoul 135-710, Republic of Korea

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indicate that the action of metformin on the gut endocrine system may be L-cell-specific and, more precisely, GLP1-specific, and may be distinct from DPP4 inhibition. Recently, it has been reported that the insulin and Wnt signaling pathways converge their

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Emily G Farrow
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Lelia J Summers
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Susan C Schiavi Department of Medical and Molecular Genetics, Genzyme, Oregon Health and Science University, Indiana University School of Medicine, 975 West Walnut Street, IB130, Indianapolis, Indiana 46202, USA

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James A McCormick Department of Medical and Molecular Genetics, Genzyme, Oregon Health and Science University, Indiana University School of Medicine, 975 West Walnut Street, IB130, Indianapolis, Indiana 46202, USA

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David H Ellison Department of Medical and Molecular Genetics, Genzyme, Oregon Health and Science University, Indiana University School of Medicine, 975 West Walnut Street, IB130, Indianapolis, Indiana 46202, USA

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Kenneth E White
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renal Wnt signaling To screen for novel pathways involved in renal FGF23-dependent signaling, PCR-based array technology was utilized in initial experiments. This Pathway-Finder array contains primers recognizing 84 genes from 18 signaling pathways

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Spyridon Champeris Tsaniras Diabetes Research Group, Division of Reproduction and Endocrinology, King's College London, Hodgkin Building (2.10N), Guy's Campus, London SE1 1UL, UK

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Peter M Jones Diabetes Research Group, Division of Reproduction and Endocrinology, King's College London, Hodgkin Building (2.10N), Guy's Campus, London SE1 1UL, UK

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differentiation process. In this review, we will attempt to clarify the use of these media supplements by focusing on the specific signaling pathways through which they operate, predominantly the PI3K, transforming growth factor β (TGFβ), Wnt/β-catenin, Hedgehog

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Ghania Ramdani Department of Medicine, University of California, San Diego, La Jolla, California, USA

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Nadine Schall Department of Medicine, University of California, San Diego, La Jolla, California, USA
The Institute for Pharmacology and Toxicology, University of Bonn, Bonn, Germany

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Hema Kalyanaraman Department of Medicine, University of California, San Diego, La Jolla, California, USA

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Nisreen Wahwah Department of Medicine, University of California, San Diego, La Jolla, California, USA

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Sahar Moheize Department of Medicine, University of California, San Diego, La Jolla, California, USA

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Jenna J Lee Department of Bioengineering, University of California, San Diego, La Jolla, California, USA

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Robert L Sah Department of Bioengineering, University of California, San Diego, La Jolla, California, USA

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Alexander Pfeifer The Institute for Pharmacology and Toxicology, University of Bonn, Bonn, Germany

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Darren E Casteel Department of Medicine, University of California, San Diego, La Jolla, California, USA

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Renate B Pilz Department of Medicine, University of California, San Diego, La Jolla, California, USA

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-catenin and Wnt/β-catenin-related gene expression. The sexual dimorphism of Col1a1- Prkg2 RQ transgenic mice likely relates to cross-talk between ER-α, NO/cGMP and Wnt/β-catenin signaling pathways ( Kouzmenko et al. 2004 , Mendelsohn & Karas 2010

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Tianru Jin Departments of Medicine, Division of Cell and Molecular Biology, Physiology, and Laboratory Medicine and Pathobiology, University of Toronto, Toronto, Ontario, Canada
Departments of Medicine, Division of Cell and Molecular Biology, Physiology, and Laboratory Medicine and Pathobiology, University of Toronto, Toronto, Ontario, Canada

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, intestinal but not pancreatic gcg expression was shown to be regulated by the effectors of the Wnt signaling pathway ( Ni et al . 2003 , Yi et al . 2005 ). Furthermore, insulin at pathological concentrations was shown to stimulate intestinal gcg mRNA and

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Juan Pedro Martinez-Barbera Developmental Biology and Cancer Programme, Institute of Child Health, Birth Defects Research Centre, University College London, 30 Guilford Street, WC1N 1EH London, UK

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human ACP revealed an association with mutations in CTNNB1 , the gene that encodes β-catenin, a central regulator of the Wnt pathway ( Sekine et al . 2002 , Kato et al . 2004 , Buslei et al . 2005 , Oikonomou et al . 2005 , Brastianos et al

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Asmaà Fritah Institut National de la Santé et de la Recherche Médicale, U673, Hôpital Saint-Antoine, Université Pierre et Marie Curie (UPMC-Paris 6), Paris, France

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Gérard Redeuilh Institut National de la Santé et de la Recherche Médicale, U673, Hôpital Saint-Antoine, Université Pierre et Marie Curie (UPMC-Paris 6), Paris, France

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Michèle Sabbah Institut National de la Santé et de la Recherche Médicale, U673, Hôpital Saint-Antoine, Université Pierre et Marie Curie (UPMC-Paris 6), Paris, France

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Introduction The human Wnt-1-induced signalling pathway protein-2 ( WISP-2/CCN5 ) gene is located on chromosome 20 q12-q13.1 and encodes a protein belonging to the connective tissue growth factor/cysteine-rich 61/nephroblastoma over

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Amanda L Patterson Department of Obstetrics, Gynecology, and Reproductive Biology, College of Human Medicine, Michigan State University, Grand Rapids, Michigan, USA

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Jamieson Pirochta Department of Obstetrics, Gynecology, and Reproductive Biology, College of Human Medicine, Michigan State University, Grand Rapids, Michigan, USA

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Stephanie Y Tufano Department of Obstetrics, Gynecology, and Reproductive Biology, College of Human Medicine, Michigan State University, Grand Rapids, Michigan, USA

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Jose M Teixeira Department of Obstetrics, Gynecology, and Reproductive Biology, College of Human Medicine, Michigan State University, Grand Rapids, Michigan, USA

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Wnt4 was unchanged, it is unlikely. Figure 6 Schematic model of epithelial and stromal signaling pathways affected in GOF β-catenin mice during implantation and decidualization. Estradiol signals through its receptor, ERα, in the glandular

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