Induction of the p16INK4a senescence gene as a new therapeutic strategy for the treatment of rheumatoid arthritis. - Wikidata - wikimedia - TriplyDB

Induction of the p16INK4a senescence gene as a new therapeutic strategy for the treatment of rheumatoid arthritis.

Induction of the p16INK4a senescence gene as a new therapeutic strategy for the treatment of rheumatoid arthritis.

http://www.wikidata.org/entity/Q45859175

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Fibroblast biology. Role of synovial fibroblasts in the pathogenesis of rheumatoid arthritis Gene therapy in animal models of rheumatoid arthritis: are we ready for the patients?Molecular profile of synovial fibroblasts in rheumatoid arthritis depends on the stage of proliferation.Copper chelation with tetrathiomolybdate suppresses adjuvant-induced arthritis and inflammation-associated cachexia in rats.Induction of the cytokine signal regulator SOCS3/CIS3 as a therapeutic strategy for treating inflammatory arthritis The senescence-associated secretory phenotype: the dark side of tumor suppression Identification of novel biomarkers in chronic immune thrombocytopenia (ITP) by microarray-based serum protein profiling.Rheumatoid Arthritis, Immunosenescence and the Hallmarks of Aging Multiparametric and semiquantitative scoring systems for the evaluation of mouse model histopathology--a systematic review.p21Cip1 is required for the development of monocytes and their response to serum transfer-induced arthritis.A question of transformation: the synovial fibroblast in rheumatoid arthritis Gene therapy for arthritis.15-deoxy-delta(12,14)-PGJ(2) induces synoviocyte apoptosis and suppresses adjuvant-induced arthritis in rats Perspectives on the use of gene therapy for chronic joint diseases.Gene transfer as a future therapy for rheumatoid arthritis.Is the mucosal route of administration essential for probiotic function? Subcutaneous administration is associated with attenuation of murine colitis and arthritis A cell-cycle independent role for p21 in regulating synovial fibroblast migration in rheumatoid arthritis Interactions between IL-32 and tumor necrosis factor alpha contribute to the exacerbation of immune-inflammatory diseases.Cyclin-dependent kinase inhibitor p21, via its C-terminal domain, is essential for resolution of murine inflammatory arthritis Gene therapy for autoimmune diseases: quo vadis?Detection of autoantibodies to citrullinated BiP in rheumatoid arthritis patients and pro-inflammatory role of citrullinated BiP in collagen-induced arthritis.Targets of immune regeneration in rheumatoid arthritis.miR-146b-5p mediates p16-dependent repression of IL-6 and suppresses paracrine procarcinogenic effects of breast stromal fibroblasts Actin cytoskeleton dynamics linked to synovial fibroblast activation as a novel pathogenic principle in TNF-driven arthritis.Molecular aspects of rheumatoid arthritis: role of transcription factors.Hypervariable genes--experimental error or hidden dynamics.Disorders in angiogenesis and redox pathways are main factors contributing to the progression of rheumatoid arthritis: a comparative proteomics study.Angiostatin gene transfer as an effective treatment strategy in murine collagen-induced arthritis.Inflammation and bone destruction in arthritis: synergistic activity of immune and mesenchymal cells in joints.Overexpression of SPACIA1/SAAL1, a newly identified gene that is involved in synoviocyte proliferation, accelerates the progression of synovitis in mice and humans.Histone deacetylase inhibitors MS-275 and SAHA induced growth arrest and suppressed lipopolysaccharide-stimulated NF-kappaB p65 nuclear accumulation in human rheumatoid arthritis synovial fibroblastic E11 cells.Cell cycle regulation therapy combined with cytokine blockade enhances antiarthritic effects without increasing immune suppression.Selective in vivo and in vitro effects of a small molecule inhibitor of cyclin-dependent kinase 4.Suppression of arthritis by forced expression of cyclin-dependent kinase inhibitor p21(Cip1) gene into the joints.Paradoxical effects of tissue inhibitor of metalloproteinases 1 gene transfer in collagen-induced arthritis.Inhibition of cartilage destruction by double gene transfer of IL-1Ra and IL-10 involves the activin pathway.Recombinant human endostatin inhibits adjuvant arthritis by down-regulating VEGF expression and suppression of TNF-α, IL-1β production.Evening primrose oil and celecoxib inhibited pathological angiogenesis, inflammation, and oxidative stress in adjuvant-induced arthritis: novel role of angiopoietin-1.Origins of fibroblasts in rheumatoid synovial tissues: Implications from organ fibrotic models.Obesity and p16INK4A Downregulation Activate Breast Adipocytes and Promote Their Protumorigenicity.

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Induction of the p16INK4a senescence gene as a new therapeutic strategy for the treatment of rheumatoid arthritis.

http://www.wikidata.org/entity/Q45859175

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1999 nî lūn-bûn

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Induction of the p16INK4a sene ...... tment of rheumatoid arthritis.

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Induction of the p16INK4a sene ...... tment of rheumatoid arthritis.

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type

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Induction of the p16INK4a sene ...... tment of rheumatoid arthritis.

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Induction of the p16INK4a sene ...... tment of rheumatoid arthritis.

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Induction of the p16INK4a sene ...... tment of rheumatoid arthritis.

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Induction of the p16INK4a sene ...... tment of rheumatoid arthritis.

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Induction of the p16INK4a sene ...... tment of rheumatoid arthritis.

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Hirokawa K

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Inoue N

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Ito H

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Growth suppression by p18, a p16INK4/MTS1- and p14INK4B/MTS2-related CDK6 inhibitor, correlates with wild-type pRb function

Cloning of p27Kip1, a cyclin-dependent kinase inhibitor and a potential mediator of extracellular antimitogenic signals

p15INK4B is a potential effector of TGF-beta-induced cell cycle arrest

Regulation of p16CDKN2 expression and its implications for cell immortalization and senescence

Novel INK4 proteins, p19 and p18, are specific inhibitors of the cyclin D-dependent kinases CDK4 and CDK6

The American Rheumatism Association 1987 revised criteria for the classification of rheumatoid arthritis

Deletions of the cyclin-dependent kinase-4 inhibitor gene in multiple human cancers

A cell cycle regulator potentially involved in genesis of many tumor types

p21 is a universal inhibitor of cyclin kinases

The shared epitope hypothesis. An approach to understanding the molecular genetics of susceptibility to rheumatoid arthritis

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