Đang chuẩn bị liên kết để tải về tài liệu:
Báo cáo y học: "JNK1 is not essential for TNF-mediated joint disease"

Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học General Psychiatry cung cấp cho các bạn kiến thức về ngành y đề tài:JNK1 is not essential for TNF-mediated joint disease. | Available online http arthritis-research.eom content 7 1 R166 Research article JNK1 is not essential for TNF-mediated joint disease Marcus Koller1 Silvia Hayer2 Kurt Redlich1 Romeo Ricci3 Jean-Pierre David3 Gunter Steiner1 2 Josef S Smolen1 2 Erwin F Wagner3 and Georg Schett1 Open Access Department of Internal Medicine III Division of Rheumatology Medical University of Vienna Austria 2CeMM Center of Molecular Medicine of the Austrian Academy of Sciences Vienna Austria 3Research Institute of Molecular Pathology Vienna Austria Contributed equally Corresponding author Georg Schett Georg.Schett@meduniwien.ac.at Received 4 Aug 2004 Revisions requested 26 Aug 2004 Revisions received 14 Oct 2004 Accepted 10 Nov 2004 Published 7 Dec 2004 Arthritis Res Ther 2005 7 R166-R173 DOI 10.1186 ar1473 2004 Koller et al. licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License http creativecommons.org licenses by 2.0 which permits unrestricted use distribution and reproduction in any medium provided the original work is cited. Abstract Tumour necrosis factor TNF signalling molecules are considered as promising therapeutic targets of antirheumatic therapy. Among them mitogen-activated protein kinases are thought to be of central importance. Herein we investigate the role in vivo of TNF-a signalling through c-Jun N-terminal kinase JNK 1 in destructive arthritis. Human TNF transgenic hTNFtg mice which develop inflammatory arthritis were intercrossed with JNK1-deficient JNK1 mice. Animals n 35 of all four genotypes wild-type JNK1 hTNFtg JNK1 hTNFtg were assessed for clinical and histological signs of arthritis. Clinical features of arthritis swelling and decreased grip strength developed equally in hTNFtg and JNKr hTNFtg mice. Histological analyses revealed no differences in the quantity of synovial inflammation and bone erosions or in the cellular composition of the synovial infiltrate. Bone destruction and .