title: [Regulation of apoptosis in aggressive fibroblasts].
abstract: Apoptosis is a central physiological mechanism for maintaining cellular stability in tissue. Synovial fibroblasts, which play a central role in the pathogenesis of rheumatoid arthritis (RA), show a resistance to apoptosis. Several molecular mechanisms are involved in such resistance. Thus, soluble Fas can bind Fas ligands (Fas-L) and hinder Fas-L induced apoptosis in fibroblasts. SUMO-1 (a small ubiquitin-like modifier) attaches to proteins post-translationally. This appears to be significantly involved in apoptosis resistance in RA fibroblasts. SUMO-1 levels are substantially increased in synovial fibroblasts from RA patients. A change in the post-translational SUMOlation pattern could represent a new target for changing the stable activation of synovial fibroblasts in RA.
authors: Bereich Molekulare Medizin des Muskuloskeletalen Systems, Universitätsklinikum Münster, Domagkstrasse 3, 48149 Münster. thomas.pap@uni-muenster.de
authors: T
authors: T
authors: Pap
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000276:immunology*; D001172:Arthritis, Rheumatoid / Q000276:immunology* / Q000473:pathology*; D005347:Fibroblasts / Q000276:immunology*; D006801:Humans; D018448:Models, Immunological; D025842:SUMO-1 Protein / Q000276:immunology*; D013583:Synovial Membrane / Q000276:immunology* / Q000473:pathology
chemical_list: D025842:SUMO-1 Protein