TGF-beta/Smad3 signals repress chondrocyte hypertrophic differentiation and are required for maintaining articular cartilage - Wikidata - wikimedia - TriplyDB

TGF-beta/Smad3 signals repress chondrocyte hypertrophic differentiation and are required for maintaining articular cartilage

TGF-beta/Smad3 signals repress chondrocyte hypertrophic differentiation and are required for maintaining articular cartilage

http://www.wikidata.org/entity/Q36342408

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Mechanisms for asporin function and regulation in articular cartilage Smad3 prevents beta-catenin degradation and facilitates beta-catenin nuclear translocation in chondrocytes A functional SNP in CILP, encoding cartilage intermediate layer protein, is associated with susceptibility to lumbar disc disease SMAD3 deficiency promotes inflammatory aortic aneurysms in angiotensin II-infused mice via activation of iNOS Adult mesenchymal stem cells and cell-based tissue engineering BMP receptor signaling is required for postnatal maintenance of articular cartilage The Smads TGF-β and BMP signaling in osteoblast, skeletal development, and bone formation, homeostasis and disease Wnts talking with the TGF-β superfamily: WISPers about modulation of osteoarthritis Advances in understanding cartilage remodeling The Regulatory Role of Signaling Crosstalk in Hypertrophy of MSCs and Human Articular Chondrocytes Interplay between cartilage and subchondral bone contributing to pathogenesis of osteoarthritis Osteoarthritis pathogenesis: a review of molecular mechanisms Doxorubicin-mediated bone loss in breast cancer bone metastases is driven by an interplay between oxidative stress and induction of TGFβ 24R,25-Dihydroxyvitamin D3 Protects against Articular Cartilage Damage following Anterior Cruciate Ligament Transection in Male Rats Interaction of TGFβ and BMP signaling pathways during chondrogenesis Bone morphogenetic proteins 2 and 6, expressed in arthritic synovium, are regulated by proinflammatory cytokines and differentially modulate fibroblast-like synoviocyte apoptosis Follistatin-like protein 1 regulates chondrocyte proliferation and chondrogenic differentiation of mesenchymal stem cells Expression and regulation of the osteoarthritis-associated protein asporin An aspartic acid repeat polymorphism in asporin inhibits chondrogenesis and increases susceptibility to osteoarthritis Lung alveolar septation defects in Ltbp-3-null mice Developmentally regulated expression of mouse HtrA3 and its role as an inhibitor of TGF-beta signaling Functional knockout of the matrilin-3 gene causes premature chondrocyte maturation to hypertrophy and increases bone mineral density and osteoarthritis Axin2 regulates chondrocyte maturation and axial skeletal development Bone abnormalities in latent TGF-[beta] binding protein (Ltbp)-3-null mice indicate a role for Ltbp-3 in modulating TGF-[beta] bioavailability Anti-transforming growth factor ß antibody treatment rescues bone loss and prevents breast cancer metastasis to bone Pharmacologic inhibition of the TGF-beta type I receptor kinase has anabolic and anti-catabolic effects on bone.SnoN suppresses maturation of chondrocytes by mediating signal cross-talk between transforming growth factor-β and bone morphogenetic protein pathways.Filamin B represses chondrocyte hypertrophy in a Runx2/Smad3-dependent manner.Inhibition of TGF-β signaling in mesenchymal stem cells of subchondral bone attenuates osteoarthritis Inhibition of ALK5 signaling induces physeal dysplasia in rats.Identification of unique molecular subdomains in the perichondrium and periosteum and their role in regulating gene expression in the underlying chondrocytes Molecular profiling of the developing mouse axial skeleton: a role for Tgfbr2 in the development of the intervertebral disc.AIMP1 downregulation restores chondrogenic characteristics of dedifferentiated/degenerated chondrocytes by enhancing TGF-β signal.Biglycan and fibromodulin have essential roles in regulating chondrogenesis and extracellular matrix turnover in temporomandibular joint osteoarthritis.Integrin α1β1 differentially regulates cytokine-mediated responses in chondrocytes.SMAD3 is associated with the total burden of radiographic osteoarthritis: the Chingford study.Smad signaling in skeletal development and regeneration.Conditional removal of the canonical TGF-β1 signaling delays condylar cartilage degeneration induced by a partial discectomy in mice MicroRNA-146a regulates human foetal femur derived skeletal stem cell differentiation by down-regulating SMAD2 and SMAD3.

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TGF-beta/Smad3 signals repress chondrocyte hypertrophic differentiation and are required for maintaining articular cartilage

http://www.wikidata.org/entity/Q36342408

description

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TGF-beta/Smad3 signals repress ...... aintaining articular cartilage

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TGF-beta/Smad3 signals repress ...... aintaining articular cartilage

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TGF-beta/Smad3 signals repress ...... aintaining articular cartilage

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TGF-beta/Smad3 signals repress ...... aintaining articular cartilage

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TGF-beta/Smad3 signals repress ...... aintaining articular cartilage

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P2860

TGF-beta signal transduction

MADR2 is a substrate of the TGFbeta receptor and its phosphorylation is required for nuclear accumulation and signaling

TGF-beta receptor-mediated signalling through Smad2, Smad3 and Smad4

MADR2 maps to 18q21 and encodes a TGFbeta-regulated MAD-related protein that is functionally mutated in colorectal carcinoma

Receptor-associated Mad homologues synergize as effectors of the TGF-beta response

Fibroblast growth factor receptor 3 is a negative regulator of bone growth

Indian hedgehog signaling regulates proliferation and differentiation of chondrocytes and is essential for bone formation

TGF-beta signalling from cell membrane to nucleus through SMAD proteins

The family of bone morphogenetic proteins

The Bmp8 gene is expressed in developing skeletal tissue and maps near the Achondroplasia locus on mouse chromosome 4

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