Loss of wnt/β-catenin signaling causes cell fate shift of preosteoblasts from osteoblasts to adipocytes - Wikidata - wikimedia - TriplyDB

Loss of wnt/β-catenin signaling causes cell fate shift of preosteoblasts from osteoblasts to adipocytes

Loss of wnt/β-catenin signaling causes cell fate shift of preosteoblasts from osteoblasts to adipocytes

http://www.wikidata.org/entity/Q36328528

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Cellular Reprogramming Using Defined Factors and MicroRNAs Mesenchymal progenitors and the osteoblast lineage in bone marrow hematopoietic niches Wnt-Lrp5 signaling regulates fatty acid metabolism in the osteoblast.The role of nuclear factor I-C in tooth and bone development.Bone marrow fat accumulation accelerated by high fat diet is suppressed by exercise.Osterix marks distinct waves of primitive and definitive stromal progenitors during bone marrow development.Kruppel-like factor 4 attenuates osteoblast formation, function, and cross talk with osteoclasts Loss of Gsα early in the osteoblast lineage favors adipogenic differentiation of mesenchymal progenitors and committed osteoblast precursors.Exercise Regulation of Marrow Fat in the Setting of PPARγ Agonist Treatment in Female C57BL/6 Mice.mTOR inhibition rescues osteopenia in mice with systemic sclerosis.Increased glutamine catabolism mediates bone anabolism in response to WNT signaling Osterix-Cre transgene causes craniofacial bone development defect A Comprehensive Overview of Skeletal Phenotypes Associated with Alterations in Wnt/β-catenin Signaling in Humans and Mice.The regulation of osteoclast differentiation by Wnt signals Pathophysiological role of enhanced bone marrow adipogenesis in diabetic complications.Sclerostin antibody treatment improves fracture outcomes in a Type I diabetic mouse model.Curcumin alleviates glucocorticoid-induced osteoporosis through the regulation of the Wnt signaling pathway.Loss of Gsα in the Postnatal Skeleton Leads to Low Bone Mass and a Blunted Response to Anabolic Parathyroid Hormone Therapy Estrogen receptor-α signaling in osteoblast progenitors stimulates cortical bone accrual Cysteine Dioxygenase Type 1 Inhibits Osteogenesis by Regulating Wnt Signaling in Primary Mouse Bone Marrow Stromal Cells.Hdac3 Deficiency Increases Marrow Adiposity and Induces Lipid Storage and Glucocorticoid Metabolism in Osteochondroprogenitor Cells Single cell gene expression profiling of cortical osteoblast lineage cells.Disruption of Wnt/β-catenin signaling in odontoblasts and cementoblasts arrests tooth root development in postnatal mouse teeth.Increased Gs Signaling in Osteoblasts Reduces Bone Marrow and Whole-Body Adiposity in Male Mice.Suppression of EZH2 Prevents the Shift of Osteoporotic MSC Fate to Adipocyte and Enhances Bone Formation During Osteoporosis β-catenin promotes bone formation and suppresses bone resorption in postnatal growing mice.Rictor is required for optimal bone accrual in response to anti-sclerostin therapy in the mouse.Overexpression of HSPA1A enhances the osteogenic differentiation of bone marrow mesenchymal stem cells via activation of the Wnt/β-catenin signaling pathway FOXOs attenuate bone formation by suppressing Wnt signaling.Interactions between B lymphocytes and the osteoblast lineage in bone marrow.Basic biology of skeletal aging: role of stress response pathways.GDF11 decreases bone mass by stimulating osteoclastogenesis and inhibiting osteoblast differentiation.SOX2 regulates YAP1 to maintain stemness and determine cell fate in the osteo-adipo lineage.β-catenin activity in late hypertrophic chondrocytes locally orchestrates osteoblastogenesis and osteoclastogenesis.CathepsinKCre mediated deletion of βcatenin results in dramatic loss of bone mass by targeting both osteoclasts and osteoblastic cells.Wnt and the Wnt signaling pathway in bone development and disease.Pyrroloquinoline quinone prevents testosterone deficiency-induced osteoporosis by stimulating osteoblastic bone formation and inhibiting osteoclastic bone resorption.Osteoblast recruitment to sites of bone formation in skeletal development, homeostasis, and regeneration.Bone cell senescence: mechanisms and perspectives.Low bone turnover and reduced angiogenesis in streptozotocin-induced osteoporotic mice.

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Loss of wnt/β-catenin signaling causes cell fate shift of preosteoblasts from osteoblasts to adipocytes

http://www.wikidata.org/entity/Q36328528

description

2012 nî lūn-bûn

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2012年の論文

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2012年学术文章

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2012年学术文章

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2012年学术文章

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2012年学术文章

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2012年學術文章

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2012年學術文章

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2012年學術文章

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name

Loss of wnt/β-catenin signalin ...... from osteoblasts to adipocytes

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Loss of wnt/β-catenin signalin ...... from osteoblasts to adipocytes

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type

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Loss of wnt/β-catenin signalin ...... from osteoblasts to adipocytes

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Loss of wnt/β-catenin signalin ...... from osteoblasts to adipocytes

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prefLabel

Loss of wnt/β-catenin signalin ...... from osteoblasts to adipocytes

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Loss of wnt/β-catenin signalin ...... from osteoblasts to adipocytes

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Journal of Bone and Mineral Research

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Loss of wnt/β-catenin signalin ...... from osteoblasts to adipocytes

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F Richard Bringhurst

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Henry M Kronenberg

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Jun Guo

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Lige Song

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Minlin Liu

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Noriaki Ono

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P2860

Inhibition of adipogenesis by Wnt signaling

The novel zinc finger-containing transcription factor osterix is required for osteoblast differentiation and bone formation

Skeletal alterations in rats during space flight

Wnt/beta-catenin signaling in mesenchymal progenitors controls osteoblast and chondrocyte differentiation during vertebrate skeletogenesis

Canonical Wnt signaling in differentiated osteoblasts controls osteoclast differentiation

Canonical Wnt/beta-catenin signaling prevents osteoblasts from differentiating into chondrocytes

Regulation of osteoblastogenesis and bone mass by Wnt10b

Sequential roles of Hedgehog and Wnt signaling in osteoblast development

Wnt10b increases postnatal bone formation by enhancing osteoblast differentiation

Inactivation of the beta-catenin gene by Wnt1-Cre-mediated deletion results in dramatic brain malformation and failure of craniofacial development

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10.1002/JBMR.1694

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11

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27

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3474875

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