Molecular and cellular mechanisms of joint destruction in rheumatoid arthritis: two cellular mechanisms explain joint destruction? - Wikidata - awgldk - TriplyDB

Molecular and cellular mechanisms of joint destruction in rheumatoid arthritis: two cellular mechanisms explain joint destruction?

Molecular and cellular mechanisms of joint destruction in rheumatoid arthritis: two cellular mechanisms explain joint destruction?

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Kinesin-like protein CENP-E is upregulated in rheumatoid synovial fibroblasts Fibroblast biology. Role of synovial fibroblasts in the pathogenesis of rheumatoid arthritis High CXCR3 expression in synovial mast cells associated with CXCL9 and CXCL10 expression in inflammatory synovial tissues of patients with rheumatoid arthritis Association of a specific haplotype across the genes MMP1 and MMP3 with radiographic joint destruction in rheumatoid arthritis Intra-articular injections of high-molecular-weight hyaluronic acid have biphasic effects on joint inflammation and destruction in rat antigen-induced arthritis.Characterization of histopathology and gene-expression profiles of synovitis in early rheumatoid arthritis using targeted biopsy specimens.Human cathepsin O2, a novel cysteine protease highly expressed in osteoclastomas and ovary molecular cloning, sequencing and tissue distribution Identification of autoantibodies against transthyretin for the screening and diagnosis of rheumatoid arthritis Retroviral sequences in rheumatoid arthritis synovium.Tyrosine phosphorylated proteins in synovial cells of rheumatoid arthritis.Reduction of IL-20 Expression in Rheumatoid Arthritis by Linear Polarized Infrared Light Irradiation Joint damage in rheumatoid arthritis progresses in remission according to the Disease Activity Score in 28 joints and is driven by residual swollen joints.Regional analysis of p53 mutations in rheumatoid arthritis synovium Tachykinin receptor modulators: novel therapeutics for rheumatoid arthritis.Gene expression analysis of rheumatoid arthritis synovial lining regions by cDNA microarray combined with laser microdissection: up-regulation of inflammation-associated STAT1, IRF1, CXCL9, CXCL10, and CCL5.Selected reaction monitoring to differentiate and relatively quantitate isomers of sulfated and unsulfated core 1 O-glycans from salivary MUC7 protein in rheumatoid arthritis.Rheumatoid arthritis and tumor necrosis factor alpha.Attenuation of murine antigen-induced arthritis by treatment with a decoy oligodeoxynucleotide inhibiting signal transducer and activator of transcription-1 (STAT-1).Identification of blood biomarkers of rheumatoid arthritis by transcript profiling of peripheral blood mononuclear cells from the rat collagen-induced arthritis model.Reduction of interleukin-6 expression in human synoviocytes and rheumatoid arthritis rat joints by linear polarized near infrared light (Superlizer) irradiation.Reduction of monocyte chemoattractant protein-1 expression in rheumatoid arthritis rat joints with light-emitting diode phototherapy.p53 in rheumatoid arthritis synovial fibroblasts at sites of invasion.TNF receptor gene therapy results in suppression of IgG2a anticollagen antibody in collagen induced arthritis.Perpetuation of inflammation associated with experimental arthritis: the role of macrophage activation by neutrophilic myeloperoxidase.Trichostatin A sensitises rheumatoid arthritis synovial fibroblasts for TRAIL-induced apoptosis Cartilage destruction mediated by synovial fibroblasts does not depend on proliferation in rheumatoid arthritis Mesenchymal stromal cells. Nurse-like cells reside in the synovial tissue and bone marrow in rheumatoid arthritis.Toll-like receptors in rheumatoid arthritis joint destruction mediated by two distinct pathways.Synovial fibroblasts: key players in rheumatoid arthritis.Cells of the synovium in rheumatoid arthritis. Synovial fibroblasts.Mechanisms of disease: the molecular and cellular basis of joint destruction in rheumatoid arthritis.Somatic mutations in the p53 tumor suppressor gene in rheumatoid arthritis synovium.Modulation of Apoptosis and Differentiation by the Treatment of Sulfasalazine in Rabbit Articular Chondrocytes.Developments in the clinical understanding of rheumatoid arthritis.Susceptibility of rheumatoid arthritis synovial fibroblasts to FasL- and TRAIL-induced apoptosis is cell cycle-dependent.15-deoxy-Delta 12,14-ProstaglandinJ2 regulates dedifferentiation through peroxisome proliferator-activated receptor-gamma-dependent pathway but not COX-2 expression in articular chondrocytes.ERK-1/-2 and p38 kinase oppositely regulate 15-deoxy-delta(12,14)-prostaglandinJ(2)-Induced PPAR-gamma activation that mediates dedifferentiation but not cyclooxygenase-2 expression in articular chondrocytes.Simvastatin induces apoptosis of fibroblast-like synoviocytes Gene expression profiling of rheumatoid arthritis synovial cells treated with antirheumatic drugs.Effects of 18β-Glycyrrhetinic acid in hTNFtg mice - a model of rheumatoid arthritis.

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Molecular and cellular mechanisms of joint destruction in rheumatoid arthritis: two cellular mechanisms explain joint destruction?

http://www.wikidata.org/entity/Q40901167

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Complete nucleotide and deduced amino acid sequences of human and murine preprocathepsin L. An abundant transcript induced by transformation of fibroblasts

Tumorigenic conversion of primary embryo fibroblasts requires at least two cooperating oncogenes

Human memory T lymphocytes express increased levels of three cell adhesion molecules (LFA-3, CD2, and LFA-1) and three other molecules (UCHL1, CDw29, and Pgp-1) and have enhanced IFN-gamma production

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

The identification of active forms of cysteine proteinases in Kirsten-virus-transformed mouse fibroblasts by use of a specific radiolabelled inhibitor

The role of Jun, Fos and the AP-1 complex in cell-proliferation and transformation

Leukocyte-endothelial cell recognition: three (or more) steps to specificity and diversity

Rheumatoid factors isolated from patients with autoimmune disorders are derived from germline genes distinct from those encoding the Wa, Po, and Bla cross-reactive idiotypes.

The immunoglobulin kappa light chain repertoire expressed in the synovium of a patient with rheumatoid arthritis.

Rheumatoid arthritis complicated by infection with the human immunodeficiency virus and the development of Sjögren's syndrome.

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