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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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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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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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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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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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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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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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-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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Department of Anatomy and Structural Science, Yamagata University Faculty of Medicine, Yamagata, Japan
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WELBIO, Université Libre de Bruxelles (ULB), Brussels, 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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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
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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/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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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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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
Cátedra de Fisiología Humana, Facultad de Bioquímica y Ciencias Biológicas, Universidad Nacional del Litoral, Santa Fe, Argentina
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Cátedra de Fisiología Humana, Facultad de Bioquímica y Ciencias Biológicas, Universidad Nacional del Litoral, Santa Fe, Argentina
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Cátedra de Fisiología Humana, Facultad de Bioquímica y Ciencias Biológicas, Universidad Nacional del Litoral, Santa Fe, Argentina
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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