Immortalization and characterization of osteoblast cell lines generated from wild‐type and Nmp4‐null mouse bone marrow stromal cells using murine telomerase reverse transcriptase (mTERT) (original) (raw)

Nmp4/CIZ Suppresses the Response of Bone to Anabolic Parathyroid Hormone by Regulating Both Osteoblasts and Osteoclasts

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Nmp4/CIZ Suppresses the Parathyroid Hormone Anabolic Window by Restricting Mesenchymal Stem Cell and Osteoprogenitor Frequency

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Intermittent administration of parathyroid hormone (1‐34) stimulates matrix metalloproteinase‐9 (MMP‐9) expression in rat long bone

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Journal of Cellular Biochemistry, 1998

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Nmp4/CIZ suppresses parathyroid hormone‐induced increases in trabecular bone

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Accentuated osteoclastic response to parathyroid hormone undermines bone mass acquisition in osteonectin-null mice

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Parathyroid hormone receptor signaling induces bone resorption in the adult skeleton by directly regulating the RANKL gene in osteocytes

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Parathyroid Hormone Stimulates Osteoblastic Expression of MCP-1 to Recruit and Increase the Fusion of Pre/Osteoclasts

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Parathyroid Hormone Uses Multiple Mechanisms to Arrest the Cell Cycle Progression of Osteoblastic Cells from G1 to S Phase

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Title: Maximizing PTH Anabolic Osteoporosis Therapy

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Parathyroid hormone signaling in mature osteoblasts/osteocytes protects mice from age-related bone loss

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Faculty of 1000 evaluation for Effects of intermittent parathyroid hormone treatment on osteoprogenitor cells in postmenopausal women

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Effects of intermittent parathyroid hormone treatment on osteoprogenitor cells in postmenopausal women

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Cells of the Osteoclast Lineage as Mediators of the Anabolic Actions of Parathyroid Hormone in Bone

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Increased bone formation by prevention of osteoblast apoptosis with parathyroid hormone

Teresita Bellido

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Current perspectives on parathyroid hormone (PTH) and PTH-related protein (PTHrP) as bone anabolic therapies

Alcaraz, Maria katrina H.

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Parathyroid Hormone Stimulates Circulating Osteogenic Cells in Hypoparathyroidism

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Induction of osteoclast formation by parathyroid hormone depends on an action on stromal cells

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MMP14 is a novel target of PTH signaling in osteocytes that controls resorption by regulating soluble RANKL production

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Parathyroid hormone-dependent signaling pathways regulating genes in bone cells

N. Partridge

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Deletion of the nuclear localization sequence and C-terminus of parathyroid hormone–related protein decreases osteogenesis and chondrogenesis but increases adipogenesis and myogenesis in murine bone marrow stromal cells

Ramiro Toribio

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Are Osteoclasts Needed for the Bone Anabolic Response to Parathyroid Hormone?: A STUDY OF INTERMITTENT PARATHYROID HORMONE WITH DENOSUMAB OR ALENDRONATE IN KNOCK-IN MICE EXPRESSING HUMANIZED RANKL

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Aberrant gene expression profiles, during in vitro osteoblast differentiation, of telomerase deficient mouse bone marrow stromal stem cells (mBMSCs)

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Journal of Biomedical Science, 2015

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Chronic Elevation of Parathyroid Hormone in Mice Reduces Expression of Sclerostin by Osteocytes: A Novel Mechanism for Hormonal Control of Osteoblastogenesis

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Nmp4/CIZ regulation of matrix metalloproteinase 13 (MMP-13) response to parathyroid hormone in osteoblasts

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American Journal of Physiology-Endocrinology and Metabolism, 2004

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The C-terminal fragment of parathyroid hormone-related peptide promotes bone formation in diabetic mice with low-turnover osteopaenia

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British Journal of Pharmacology, 2011

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Parathyroid Hormone-Related Protein Is Required for Normal Intramembranous Bone Development

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Journal of Bone and Mineral Research, 2001

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Differential Regulation of Osteoblast Activity by Th Cell Subsets Mediated by Parathyroid Hormone and IFN-γ

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Parathyroid hormone regulates the distribution and osteoclastogenic potential of hematopoietic progenitors in the bone marrow

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Anabolic or Catabolic Responses of MC3T3-E1 Osteoblastic Cells to Parathyroid Hormone Depend on Time and Duration of Treatment

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Control of bone mass and remodeling by PTH receptor signaling in osteocytes

Charles O'Brien, Teresita Bellido, Lilian Plotkin

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Sustained RANKL response to parathyroid hormone in oncostatin M receptor-deficient osteoblasts converts anabolic treatment to a catabolic effect in vivo

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