The loss of Smad3 results in a lower rate of bone formation and osteopenia through dysregulation of osteoblast differentiation and apoptosis
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Loss of Smad3-mediated negative regulation of Runx2 activity leads to an alteration in cell fate determinationTIEG1 null mouse-derived osteoblasts are defective in mineralization and in support of osteoclast differentiation in vitroTGF-β and BMP signaling in osteoblast, skeletal development, and bone formation, homeostasis and diseaseRegulation of postnatal bone homeostasis by TGFβMechanisms of bone anabolism regulated by statinsDoxorubicin-mediated bone loss in breast cancer bone metastases is driven by an interplay between oxidative stress and induction of TGFβLipid metabolism disorders and bone dysfunction--interrelated and mutually regulated (review)Parathyroid hormone-responsive Smad3-related factor, Tmem119, promotes osteoblast differentiation and interacts with the bone morphogenetic protein-Runx2 pathwayParathyroid hormone-Smad3 axis exerts anti-apoptotic action and augments anabolic action of transforming growth factor beta in osteoblastsAnti-transforming growth factor ß antibody treatment rescues bone loss and prevents breast cancer metastasis to bonePharmacologic inhibition of the TGF-beta type I receptor kinase has anabolic and anti-catabolic effects on bone.Medical applications of transforming growth factor-betaTransforming growth factor-{beta} coordinately induces suppressor of cytokine signaling 3 and leukemia inhibitory factor to suppress osteoclast apoptosis.Role of TGF-β in a mouse model of high turnover renal osteodystrophy.Quantitative trait loci, genes, and polymorphisms that regulate bone mineral density in mouseMicrofibril-associated glycoprotein-1, an extracellular matrix regulator of bone remodeling.TGF-beta regulates the mechanical properties and composition of bone matrix.The G-protein-coupled receptor GPR103 regulates bone formation.PAPSS2 promotes alkaline phosphates activity and mineralization of osteoblastic MC3T3-E1 cells by crosstalk and Smads signal pathways.Conditional mesenchymal disruption of pkd1 results in osteopenia and polycystic kidney disease.PPARgamma insufficiency enhances osteogenesis through osteoblast formation from bone marrow progenitors.Promotion of osteoclast survival and antagonism of bisphosphonate-induced osteoclast apoptosis by glucocorticoids.Cilia-like structures and polycystin-1 in osteoblasts/osteocytes and associated abnormalities in skeletogenesis and Runx2 expression.Role of osteoglycin in the linkage between muscle and bone.Disruption of Kif3a in osteoblasts results in defective bone formation and osteopenia.Effects of bone matrix proteins on fracture and fragility in osteoporosis.Scar wars: is TGFbeta the phantom menace in scleroderma?Congenic mice provide in vivo evidence for a genetic locus that modulates intrinsic transforming growth factor β1-mediated signaling and bone acquisition.Granulocyte colony-stimulating factor induces osteoblast apoptosis and inhibits osteoblast differentiation.Smad4 is required for maintaining normal murine postnatal bone homeostasisProlonged alendronate treatment prevents the decline in serum TGF-β1 levels and reduces cortical bone strength in long-term estrogen deficiency rat modelCritical roles of the TGF-beta type I receptor ALK5 in perichondrial formation and function, cartilage integrity, and osteoblast differentiation during growth plate developmentDose-dependent effects of Runx2 on bone development.Osteoblastogenesis regulation signals in bone remodeling.Should we abandon statins in the prevention of bone fractures?Smad3 binds Scleraxis and Mohawk and regulates tendon matrix organization.Pharmacological and biological therapeutic strategies for osteogenesis imperfecta.Biphasic effects of transforming growth factor β on bone morphogenetic protein-induced osteoblast differentiation.Fibrosis markers, hip fracture risk, and bone density in older adults.Inhibition of insulin-like growth factor-1 (IGF-1) expression by prolonged transforming growth factor-β1 (TGF-β1) administration suppresses osteoblast differentiation
P2860
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P2860
The loss of Smad3 results in a lower rate of bone formation and osteopenia through dysregulation of osteoblast differentiation and apoptosis
description
2001 թուականի Հոկտեմբերին հրատարակուած գիտական յօդուած
@hyw
2001 թվականի հոտեմբերին հրատարակված գիտական հոդված
@hy
artículu científicu espublizáu en 2001
@ast
im Oktober 2001 veröffentlichter wissenschaftlicher Artikel
@de
scientific journal article
@en
vedecký článok (publikovaný 2001/10/01)
@sk
vědecký článek publikovaný v roce 2001
@cs
wetenschappelijk artikel (gepubliceerd op 2001/10/01)
@nl
наукова стаття, опублікована в жовтні 2001
@uk
مقالة علمية (نشرت في أكتوبر 2001)
@ar
name
The loss of Smad3 results in a ...... differentiation and apoptosis
@ast
The loss of Smad3 results in a ...... differentiation and apoptosis
@en
The loss of Smad3 results in a ...... differentiation and apoptosis
@nl
type
label
The loss of Smad3 results in a ...... differentiation and apoptosis
@ast
The loss of Smad3 results in a ...... differentiation and apoptosis
@en
The loss of Smad3 results in a ...... differentiation and apoptosis
@nl
prefLabel
The loss of Smad3 results in a ...... differentiation and apoptosis
@ast
The loss of Smad3 results in a ...... differentiation and apoptosis
@en
The loss of Smad3 results in a ...... differentiation and apoptosis
@nl
P2093
P921
P3181
P1476
The loss of Smad3 results in a ...... differentiation and apoptosis
@en
P2093
A. J. Borton
J. P. Frederick
M. B. Datto
R. S. Weinstein
X. F. Wang
P2860
P304
P3181
P356
10.1359/JBMR.2001.16.10.1754
P577
2001-10-01T00:00:00Z