Transforming growth factor (TGF)-β signalling is increased in rheumatoid synovium but TGF-β blockade does not modify experimental arthritis. - Test2 - elhamkhani - TriplyDB

Transforming growth factor (TGF)-β signalling is increased in rheumatoid synovium but TGF-β blockade does not modify experimental arthritis.

Transforming growth factor (TGF)-β signalling is increased in rheumatoid synovium but TGF-β blockade does not modify experimental arthritis.

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Smad-dependent mechanisms of inflammatory bone destruction Genetic Basis of Common Human Disease: Insight into the Role of Missense SNPs from Genome-Wide Association Studies Relationship between serum transforming growth factor β 1 concentrations and the duration of type 1 diabetes mellitus in children and adolescents Parasitic infection as a potential therapeutic tool against rheumatoid arthritis Intraarticular overexpression of Smad7 ameliorates experimental arthritis.Periploca forrestii Saponin Ameliorates Murine CFA-Induced Arthritis by Suppressing Cytokine Production.Human embryonic stem cell-derived mesenchymal stromal cells ameliorate collagen-induced arthritis by inducing host-derived indoleamine 2,3 dioxygenase Identification of a transitional fibroblast function in very early rheumatoid arthritis.Suppression of Th1 and Th17 Responses and Induction of Treg Responses by IL-18-Expressing Plasmid Gene Combined with IL-4 on Collagen-Induced Arthritis.B Cell Regulation in Autoimmune Diseases

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P2860

Transforming growth factor (TGF)-β signalling is increased in rheumatoid synovium but TGF-β blockade does not modify experimental arthritis.

http://www.wikidata.org/entity/Q44117426

description

2013 nî lūn-bûn

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2013年の論文

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2013年学术文章

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2013年学术文章

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2013年学术文章

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2013年学术文章

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2013年学术文章

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2013年学术文章

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2013年學術文章

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2013年學術文章

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Clinical and Experimental Immunology

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Transforming growth factor (TG ...... modify experimental arthritis.

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B Santiago

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E Gonzalo-Gil

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G Criado

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J L Pablos

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P2860

Transforming growth factor beta 1 null mutation in mice causes excessive inflammatory response and early death

Generation of pathogenic T(H)17 cells in the absence of TGF-β signalling

Reciprocal developmental pathways for the generation of pathogenic effector TH17 and regulatory T cells

The orphan nuclear receptor RORgammat directs the differentiation program of proinflammatory IL-17+ T helper cells

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

Targeted disruption of the mouse transforming growth factor-beta 1 gene results in multifocal inflammatory disease

Transforming growth factor-beta induces development of the T(H)17 lineage

Blocking Smad7 restores TGF-beta1 signaling in chronic inflammatory bowel disease

T helper 17 lineage differentiation is programmed by orphan nuclear receptors ROR alpha and ROR gamma

Transforming growth factor-beta inhibition reduces progression of early choroidal neovascularization lesions in rats: P17 and P144 peptides

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