ALK2 R206H mutation linked to fibrodysplasia ossificans progressiva confers constitutive activity to the BMP type I receptor and sensitizes mesenchymal cells to BMP-induced osteoblast differentiation and bone formation - Wikidata - wikimedia - TriplyDB

ALK2 R206H mutation linked to fibrodysplasia ossificans progressiva confers constitutive activity to the BMP type I receptor and sensitizes mesenchymal cells to BMP-induced osteoblast differentiation and bone formation

ALK2 R206H mutation linked to fibrodysplasia ossificans progressiva confers constitutive activity to the BMP type I receptor and sensitizes mesenchymal cells to BMP-induced osteoblast differentiation and bone formation

http://www.wikidata.org/entity/Q28265302

about

Structure of the bone morphogenetic protein receptor ALK2 and implications for fibrodysplasia ossificans progressiva TGF-β and BMP signaling in osteoblast, skeletal development, and bone formation, homeostasis and disease The biological function of type I receptors of bone morphogenetic protein in bone Modeling congenital disease and inborn errors of development in Drosophila melanogaster Overactive bone morphogenetic protein signaling in heterotopic ossification and Duchenne muscular dystrophy From mysteries to medicines: drug development for fibrodysplasia ossificans progressive Identification and characterization of regulatory elements in the promoter of ACVR1, the gene mutated in Fibrodysplasia Ossificans Progressiva.Is there a biological basis for treatment of fibrodysplasia ossificans progressiva with rosiglitazone? Potential benefits and undesired effects.Molecular consequences of the ACVR1(R206H) mutation of fibrodysplasia ossificans progressiva.Fibrodysplasia ossificans progressiva: a blueprint for metamorphosis.TGFbeta/BMP type I receptors ALK1 and ALK2 are essential for BMP9-induced osteogenic signaling in mesenchymal stem cells.Intersegmental vessel formation in zebrafish: requirement for VEGF but not BMP signalling revealed by selective and non-selective BMP antagonists.Fibrodysplasia ossificans progressiva: mechanisms and models of skeletal metamorphosis Antisense-oligonucleotide mediated exon skipping in activin-receptor-like kinase 2: inhibiting the receptor that is overactive in fibrodysplasia ossificans progressiva A novel ACVR1 mutation in the glycine/serine-rich domain found in the most benign case of a fibrodysplasia ossificans progressiva variant reported to date.Alk2 regulates early chondrogenic fate in fibrodysplasia ossificans progressiva heterotopic endochondral ossification Apyrase as a novel therapeutic inhibitor of heterotopic ossification ACVR1, a therapeutic target of fibrodysplasia ossificans progressiva, is negatively regulated by miR-148a.Fibrodysplasia ossificans progressiva: a human genetic disorder of extraskeletal bone formation, or--how does one tissue become another?The genetic pleiotropy of musculoskeletal aging.Insights into the human mesenchymal stromal/stem cell identity through integrative transcriptomic profiling The role of endothelial-mesenchymal transition in heterotopic ossification.Role of altered signal transduction in heterotopic ossification and fibrodysplasia ossificans progressiva.Neofunction of ACVR1 in fibrodysplasia ossificans progressiva.An Acvr1 R206H knock-in mouse has fibrodysplasia ossificans progressiva Common mutations in ALK2/ACVR1, a multi-faceted receptor, have roles in distinct pediatric musculoskeletal and neural orphan disorders.Augmentation of Smad-dependent BMP signaling in neural crest cells causes craniosynostosis in mice.Granting immunity to FOP and catching heterotopic ossification in the Act.High-throughput screening for modulators of ACVR1 transcription: discovery of potential therapeutics for fibrodysplasia ossificans progressiva.BMP-SMAD-ID promotes reprogramming to pluripotency by inhibiting p16/INK4A-dependent senescence.Fibrodysplasia ossificans progressiva: diagnosis, management, and therapeutic horizons Investigations of activated ACVR1/ALK2, a bone morphogenetic protein type I receptor, that causes fibrodysplasia ossificans progressiva.In situ guided tissue regeneration in musculoskeletal diseases and aging : Implementing pathology into tailored tissue engineering strategies.In vitro analyses of the dysregulated R206H ALK2 kinase-FKBP12 interaction associated with heterotopic ossification in FOP.Signaling pathways regulating cartilage growth plate formation and activity.Signaling Receptors for TGF-β Family Members.Structural Basis of Intracellular TGF-β Signaling: Receptors and Smads.Bisindoylmaleimide I enhances osteogenic differentiation.Application of human induced pluripotent stem cells to model fibrodysplasia ossificans progressiva.Fas-associated factor 1 antagonizes Wnt signaling by promoting β-catenin degradation.

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ALK2 R206H mutation linked to fibrodysplasia ossificans progressiva confers constitutive activity to the BMP type I receptor and sensitizes mesenchymal cells to BMP-induced osteoblast differentiation and bone formation

http://www.wikidata.org/entity/Q28265302

description

2010 nî lūn-bûn

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2010 թուականի Յունիսին հրատարակուած գիտական յօդուած

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2010 թվականի հունիսին հրատարակված գիտական հոդված

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2010年の論文

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2010年論文

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2010年論文

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2010年論文

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2010年论文

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Journal of Bone and Mineral Research

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David J J de Gorter

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Jan de Boer

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Joyce Doorn

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Maarten van Dinther

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Marie-José Goumans

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Nils Visser

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Peter ten Dijke

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1208-15

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2015284

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10.1359/JBMR.091110

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25

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40022919

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19929436

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fibrodysplasia ossificans progressiva