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Joshua Columbus Department of Physiology, Division of Cell and Molecular Biology, Department of Medicine, Division of Endocrinology and Metabolism, Department of Laboratory Medicine and Pathobiology, Department of Nutrition, University of Toronto, Toronto, Ontario, Canada M5S 1A8
Department of Physiology, Division of Cell and Molecular Biology, Department of Medicine, Division of Endocrinology and Metabolism, Department of Laboratory Medicine and Pathobiology, Department of Nutrition, University of Toronto, Toronto, Ontario, Canada M5S 1A8

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YuTing Chiang Department of Physiology, Division of Cell and Molecular Biology, Department of Medicine, Division of Endocrinology and Metabolism, Department of Laboratory Medicine and Pathobiology, Department of Nutrition, University of Toronto, Toronto, Ontario, Canada M5S 1A8
Department of Physiology, Division of Cell and Molecular Biology, Department of Medicine, Division of Endocrinology and Metabolism, Department of Laboratory Medicine and Pathobiology, Department of Nutrition, University of Toronto, Toronto, Ontario, Canada M5S 1A8

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Weijuan Shao Department of Physiology, Division of Cell and Molecular Biology, Department of Medicine, Division of Endocrinology and Metabolism, Department of Laboratory Medicine and Pathobiology, Department of Nutrition, University of Toronto, Toronto, Ontario, Canada M5S 1A8

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Nina Zhang Department of Physiology, Division of Cell and Molecular Biology, Department of Medicine, Division of Endocrinology and Metabolism, Department of Laboratory Medicine and Pathobiology, Department of Nutrition, University of Toronto, Toronto, Ontario, Canada M5S 1A8
Department of Physiology, Division of Cell and Molecular Biology, Department of Medicine, Division of Endocrinology and Metabolism, Department of Laboratory Medicine and Pathobiology, Department of Nutrition, University of Toronto, Toronto, Ontario, Canada M5S 1A8

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Dingyan Wang Department of Physiology, Division of Cell and Molecular Biology, Department of Medicine, Division of Endocrinology and Metabolism, Department of Laboratory Medicine and Pathobiology, Department of Nutrition, University of Toronto, Toronto, Ontario, Canada M5S 1A8

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Herbert Y Gaisano Department of Physiology, Division of Cell and Molecular Biology, Department of Medicine, Division of Endocrinology and Metabolism, Department of Laboratory Medicine and Pathobiology, Department of Nutrition, University of Toronto, Toronto, Ontario, Canada M5S 1A8
Department of Physiology, Division of Cell and Molecular Biology, Department of Medicine, Division of Endocrinology and Metabolism, Department of Laboratory Medicine and Pathobiology, Department of Nutrition, University of Toronto, Toronto, Ontario, Canada M5S 1A8

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Qinghua Wang Department of Physiology, Division of Cell and Molecular Biology, Department of Medicine, Division of Endocrinology and Metabolism, Department of Laboratory Medicine and Pathobiology, Department of Nutrition, University of Toronto, Toronto, Ontario, Canada M5S 1A8
Department of Physiology, Division of Cell and Molecular Biology, Department of Medicine, Division of Endocrinology and Metabolism, Department of Laboratory Medicine and Pathobiology, Department of Nutrition, University of Toronto, Toronto, Ontario, Canada M5S 1A8
Department of Physiology, Division of Cell and Molecular Biology, Department of Medicine, Division of Endocrinology and Metabolism, Department of Laboratory Medicine and Pathobiology, Department of Nutrition, University of Toronto, Toronto, Ontario, Canada M5S 1A8

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David M Irwin Department of Physiology, Division of Cell and Molecular Biology, Department of Medicine, Division of Endocrinology and Metabolism, Department of Laboratory Medicine and Pathobiology, Department of Nutrition, University of Toronto, Toronto, Ontario, Canada M5S 1A8

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Tianru Jin Department of Physiology, Division of Cell and Molecular Biology, Department of Medicine, Division of Endocrinology and Metabolism, Department of Laboratory Medicine and Pathobiology, Department of Nutrition, University of Toronto, Toronto, Ontario, Canada M5S 1A8
Department of Physiology, Division of Cell and Molecular Biology, Department of Medicine, Division of Endocrinology and Metabolism, Department of Laboratory Medicine and Pathobiology, Department of Nutrition, University of Toronto, Toronto, Ontario, Canada M5S 1A8
Department of Physiology, Division of Cell and Molecular Biology, Department of Medicine, Division of Endocrinology and Metabolism, Department of Laboratory Medicine and Pathobiology, Department of Nutrition, University of Toronto, Toronto, Ontario, Canada M5S 1A8
Department of Physiology, Division of Cell and Molecular Biology, Department of Medicine, Division of Endocrinology and Metabolism, Department of Laboratory Medicine and Pathobiology, Department of Nutrition, University of Toronto, Toronto, Ontario, Canada M5S 1A8
Department of Physiology, Division of Cell and Molecular Biology, Department of Medicine, Division of Endocrinology and Metabolism, Department of Laboratory Medicine and Pathobiology, Department of Nutrition, University of Toronto, Toronto, Ontario, Canada M5S 1A8
Department of Physiology, Division of Cell and Molecular Biology, Department of Medicine, Division of Endocrinology and Metabolism, Department of Laboratory Medicine and Pathobiology, Department of Nutrition, University of Toronto, Toronto, Ontario, Canada M5S 1A8

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Introduction The major effector of the canonical Wnt signaling pathway is the bipartite transcription factor cat/TCF, formed by free β-catenin (β-cat) and a member of the TCF protein family (TCF-1/TCF7, LEF1, TCF-3/TCF7L1, and TCF-4/TCF7L2; Jin

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R Hardy School of Clinical and Experimental Medicine, Institute of Biomedical Research, University of Birmingham, Birmingham B15 2TT, UK

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M S Cooper School of Clinical and Experimental Medicine, Institute of Biomedical Research, University of Birmingham, Birmingham B15 2TT, UK

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signalling pathway, and the wnt antagonist dickkopf-1 (DKK1) in particular, in this effect ( Diarra et al . 2007 ). Recent studies suggest that the canonical wnt signalling pathway is central in bone development, regulating differentiation of mesenchymal

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Soo Yeon Jang Division of Endocrinology and Metabolism, Department of Internal Medicine, Korea University College of Medicine, Seoul, Korea

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Kyung Mook Choi Division of Endocrinology and Metabolism, Department of Internal Medicine, Korea University College of Medicine, Seoul, Korea

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-related proteins (sFRPs) bind to Wnt ligands, thereby inhibiting the activation of signaling pathways ( Karner & Long 2017 ). Soluble RANKL has been reported to bind to sFRP-1, a Wnt inhibitor, and ultimately induces the activation of Wnt signaling and

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

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

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Hiroto Kobayashi Department of Development and Regeneration, Cluster of Stem Cell and Developmental Biology, Unit of Stem Cell Research, KU Leuven (University of Leuven), Leuven, Belgium
Department of Anatomy and Structural Science, Yamagata University Faculty of Medicine, Yamagata, Japan

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

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Indra Van Zundert Department of Chemistry, Laboratory of Molecular Imaging and Photonics, KU Leuven, Leuven, Belgium

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Hiroshi Uji-i Department of Chemistry, Laboratory of Molecular Imaging and Photonics, KU Leuven, Leuven, Belgium

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Alizée Vercauteren Drubbel Institut de Recherche Interdisciplinaire en Biologie Humaine et Moléculaire (IRIBHM), Brussels, Belgium

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Benjamin Beck Institut de Recherche Interdisciplinaire en Biologie Humaine et Moléculaire (IRIBHM), Brussels, Belgium
WELBIO, Université Libre de Bruxelles (ULB), Brussels, Belgium

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

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

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-organize when embedded in an extracellular matrix scaffold (like Matrigel) and provided with the appropriate stem cell niche growth and regulatory factors. Typically, the Wingless-type MMTV integration site (WNT) pathway, further boosted by activation of leucine

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Gary B Silberstein Department of Molecular, Cell and Developmental Biology, Sinsheimer Laboratories, University of California, Santa Cruz, California 95064, USA

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Katharine Van Horn Department of Molecular, Cell and Developmental Biology, Sinsheimer Laboratories, University of California, Santa Cruz, California 95064, USA

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Eva Hrabeta-Robinson Department of Molecular, Cell and Developmental Biology, Sinsheimer Laboratories, University of California, Santa Cruz, California 95064, USA

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Jennifer Compton Department of Molecular, Cell and Developmental Biology, Sinsheimer Laboratories, University of California, Santa Cruz, California 95064, USA

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pathways govern the timing of the Pax-2 time-delay feedback mechanism. Furthermore, it indicates that adjustments to the timing of expression of genes such as Wnt-4 originate in the cytoplasm as well. The molecular basis for long-duration delays in

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Emin Umit Bagriacik Immunology Research Center, Department of Immunology, Department of Hematology, Endocrinology Department, Gazi University, 06500 Ankara, Turkey
Immunology Research Center, Department of Immunology, Department of Hematology, Endocrinology Department, Gazi University, 06500 Ankara, Turkey

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Melek Yaman Immunology Research Center, Department of Immunology, Department of Hematology, Endocrinology Department, Gazi University, 06500 Ankara, Turkey

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Rauf Haznedar Immunology Research Center, Department of Immunology, Department of Hematology, Endocrinology Department, Gazi University, 06500 Ankara, Turkey

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Gulsan Sucak Immunology Research Center, Department of Immunology, Department of Hematology, Endocrinology Department, Gazi University, 06500 Ankara, Turkey

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Tuncay Delibasi Immunology Research Center, Department of Immunology, Department of Hematology, Endocrinology Department, Gazi University, 06500 Ankara, Turkey

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), MYST histone acetyltransferase 2 (MYST2), neurogenin 2 (NEUROG2), sex-determining region Y (SRY)-box 1 (SOX1), sex-determining region Y (SRY)-box 2 (SOX2). (C) Gene expression for signaling pathways related to stem cell maintenance such as WNT pathway

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Anyonya R Guntur The Musculoskeletal Laboratory, Maine Medical Center Research Institute, Center for Clinical and Translational Research, 81 Research Drive, Scarborough, Maine 04074, USA

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Clifford J Rosen The Musculoskeletal Laboratory, Maine Medical Center Research Institute, Center for Clinical and Translational Research, 81 Research Drive, Scarborough, Maine 04074, USA

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/phosphatidylinositol 3-kinase (PI3K) pathways, have been the focus of recent work and both have emerged as critical for bone development, skeletal remodeling and energy metabolism. The Wnt/β-catenin pathway has been the subject of several very recent reviews ( Baron

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K A Staines
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A S Pollard
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I M McGonnell
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C Farquharson Comparative Biomedical Sciences, Roslin Institute and R(D)SVS, The Royal Veterinary College, Royal College Street, London NW1 0TU, UK

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A A Pitsillides
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control proximo–distal and anterior–posterior patterning in the growing limb bud. These two centres are regulated by signalling pathways such as Indian hedgehog (IHH) and WNT/β-catenin (reviewed elsewhere; Summerbell et al . (1973) , Kronenberg (2003

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Aijaz A John Division of Endocrinology and Centre for Research in Anabolic Skeletal Targets in Health and Illness (ASTHI), CSIR-Central Drug Research Institute, Lucknow, India

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Ravi Prakash Division of Endocrinology and Centre for Research in Anabolic Skeletal Targets in Health and Illness (ASTHI), CSIR-Central Drug Research Institute, Lucknow, India

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Divya Singh Division of Endocrinology and Centre for Research in Anabolic Skeletal Targets in Health and Illness (ASTHI), CSIR-Central Drug Research Institute, Lucknow, India

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Introduction A tight regulation of gene activation and repression is required for bone development and homeostasis. Pathways like Wnt signaling and bone morphogenetic proteins (BMPs) activate transcriptional programs of mesenchymal stem cells

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Marlise Guerrero Schimpf Instituto de Salud y Ambiente del Litoral (ISAL, UNL-CONICET), Facultad de Bioquímica y Ciencias Biológicas, Universidad Nacional del Litoral, Santa Fe, Argentina
Cátedra de Fisiología Humana, Facultad de Bioquímica y Ciencias Biológicas, Universidad Nacional del Litoral, Santa Fe, Argentina

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María M Milesi Instituto de Salud y Ambiente del Litoral (ISAL, UNL-CONICET), Facultad de Bioquímica y Ciencias Biológicas, Universidad Nacional del Litoral, Santa Fe, Argentina
Cátedra de Fisiología Humana, Facultad de Bioquímica y Ciencias Biológicas, Universidad Nacional del Litoral, Santa Fe, Argentina

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Enrique H Luque Instituto de Salud y Ambiente del Litoral (ISAL, UNL-CONICET), Facultad de Bioquímica y Ciencias Biológicas, Universidad Nacional del Litoral, Santa Fe, Argentina
Cátedra de Fisiología Humana, Facultad de Bioquímica y Ciencias Biológicas, Universidad Nacional del Litoral, Santa Fe, Argentina

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Jorgelina Varayoud Instituto de Salud y Ambiente del Litoral (ISAL, UNL-CONICET), Facultad de Bioquímica y Ciencias Biológicas, Universidad Nacional del Litoral, Santa Fe, Argentina
Cátedra de Fisiología Humana, Facultad de Bioquímica y Ciencias Biológicas, Universidad Nacional del Litoral, Santa Fe, Argentina

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included alterations in endocrine-dependent mechanisms involved in decidualization that leaded to post-implantation embryo loss. These alterations encompassed a dysregulation of ESR1-PR signaling ( Ingaramo et al. 2016 ) and Wnt pathways ( Ingaramo et al

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