Two tissue-resident progenitor lineages drive distinct phenotypes of heterotopic ossification. - Wikidata - wikimedia - TriplyDB

Two tissue-resident progenitor lineages drive distinct phenotypes of heterotopic ossification.

Two tissue-resident progenitor lineages drive distinct phenotypes of heterotopic ossification.

http://www.wikidata.org/entity/Q40459563

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Novel Model of Tendon Regeneration Reveals Distinct Cell Mechanisms Underlying Regenerative and Fibrotic Tendon Healing.Application of human induced pluripotent stem cells to model fibrodysplasia ossificans progressiva.Peripheral blood mononuclear cell immunophenotyping in fibrodysplasia ossificans progressiva patients: Evidence for monocyte DNAM1 up-regulation.A new form of IRIDA due to combined heterozygous mutations of TMPRSS6 and ACVR1A encoding the BMP receptor ALK2.Fibrodysplasia ossificans progressiva: Basic understanding and experimental models.Post-Traumatic Heterotopic Ossification: An Old Problem in Need of New Solutions.Hard targets for a second skeleton: therapeutic horizons for fibrodysplasia ossificans progressiva (FOP).Structural basis for the potent and selective binding of LDN-212854 to the BMP receptor kinase ALK2.The Expansion of Heterotopic Bone in Fibrodysplasia Ossificans Progressiva Is Activin A-Dependent.Activin-A enhances mTOR signaling to promote aberrant chondrogenesis in fibrodysplasia ossificans progressiva.Activin-dependent signaling in fibro/adipogenic progenitors causes fibrodysplasia ossificans progressiva.Animal models of fibrodysplasia ossificans progressiva.Inhibition of overactive TGF-β attenuates progression of heterotopic ossification in mice.Stem cells and heterotopic ossification: Lessons from animal models.Bone morphogenetic protein signaling mediated by ALK-2 and DLX2 regulates apoptosis in glioma-initiating cells.The Horizon of a Therapy for Rare Genetic Diseases: A "Druggable" Future for Fibrodysplasia Ossificans Progressiva.Modeling human somite development and fibrodysplasia ossificans progressiva with induced pluripotent stem cells An mTOR Signaling Modulator Suppressed Heterotopic Ossification of Fibrodysplasia Ossificans Progressiva Characterizing the Circulating Cell Populations in Traumatic Heterotopic Ossification Recent Topics in Fibrodysplasia Ossificans Progressiva Palovarotene reduces heterotopic ossification in juvenile FOP mice but exhibits pronounced skeletal toxicity

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P2860

Two tissue-resident progenitor lineages drive distinct phenotypes of heterotopic ossification.

http://www.wikidata.org/entity/Q40459563

description

2016 nî lūn-bûn

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2016年の論文

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2016年論文

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2016年論文

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2016年論文

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2016年論文

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2016年论文

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2016年论文

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2016年论文

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name

Two tissue-resident progenitor ...... s of heterotopic ossification.

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type

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Two tissue-resident progenitor ...... s of heterotopic ossification.

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Two tissue-resident progenitor ...... s of heterotopic ossification.

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SCITRANSLMED.AAF1090

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Science Translational Medicine

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Two tissue-resident progenitor ...... es of heterotopic ossification

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Agustin H Mohedas

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Amy J Wagers

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Annelies van Schie

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Arthur Lee

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Ashley J Vonner

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Charles Keller

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Devaveena Dey

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Elisabeth M W Eekhoff

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Jana Bagarova

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Joerg Ermann

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P2860

Bone formation zones in heterotopic ossifications: histologic findings and increased expression of bone morphogenetic protein 2 and transforming growth factors beta2 and beta3

A recurrent mutation in the BMP type I receptor ACVR1 causes inherited and sporadic fibrodysplasia ossificans progressiva

BMP type I receptor inhibition reduces heterotopic [corrected] ossification

Structure of the bone morphogenetic protein receptor ALK2 and implications for fibrodysplasia ossificans progressiva

ALK2 functions as a BMP type I receptor and induces Indian hedgehog in chondrocytes during skeletal development

Regulation of tendon differentiation by scleraxis distinguishes force-transmitting tendons from muscle-anchoring tendons

A global double-fluorescent Cre reporter mouse

Restoration of p53 function leads to tumour regression in vivo

Classic and atypical fibrodysplasia ossificans progressiva (FOP) phenotypes are caused by mutations in the bone morphogenetic protein (BMP) type I receptor ACVR1

Deletion of Asxl1 results in myelodysplasia and severe developmental defects in vivo

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366ra163

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10.1126/SCITRANSLMED.AAF1090

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366

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Aris Economides

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27881824

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